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PubMed1997

Functional consequences of acute collagen degradation studied in crystalloid perfused rat hearts.

OBJECTIVES: The impact of acute collagen disruption by the disulfide donor, 5,5'-dithio-2-nitrobenzoic acid (DTNB) on ventricular properties was tested in rat hearts. METHODS: Collagen was degraded acutely in 13 isolated, isovolumically contracting rat hearts by perfusion with 1 mM DTNB added to Krebs-Henseleit solution for 1 hour followed by 2-hour perfusion with normal solution. Another 13 hearts were perfused with normal solution for 3 hours (Control). RESULTS: Collagen content was 3.5 +/- 0.5% of ventricular dry weight in control group compared with 2.1 +/- 0.4% in DTNB group (decrease by 40%, p < 0.01). Scanning electron micrographs revealed loss of the delicate collagen network surrounding muscle fibers in DTNB treated hearts. Developed pressure at a fixed volume decreased to 86 +/- 17% of the baseline value after 3-hour perfusion in the control group, whereas in DTNB treated hearts developed pressure fell to 68 +/- 13% (p < 0.01). End-diastolic pressure was set at 5 mmHg at the beginning of the experiment and rose to 15 +/- 8 mmHg in control and 30 +/- 13 mmHg (p < 0.01) in the treated hearts. Concomitantly, wet-to-dry weight ratio increased from 5.63 +/- 0.26 in control to 6.07 +/- 0.11 (p < 0.05) in the DTNB treated hearts. A separate set of experiments on isolated myocytes excluded the possibility of a direct effect of DTNB on myocyte contractile function. CONCLUSIONS: These data suggested that with 40% collagen disruption by DTNB there is a significant increase in tissue edema that results in a decrease in chamber capacitance; in addition, there is a significant decrease in systolic performance which reflects the combined effect of edema and loss of collagen.

Animals↗
PubMed2000

Capacitative Ca(2+) entry and tyrosine kinase activation in canine pulmonary arterial smooth muscle cells.

We investigated the role of capacitative Ca(2+) entry and tyrosine kinase activation in mediating phenylephrine (PE)-induced oscillations in intracellular free Ca(2+) concentration ([Ca(2+)](i)) in canine pulmonary arterial smooth muscle cells (PASMCs). [Ca(2+)](i) was measured as the 340- to 380-nm ratio in individual fura 2-loaded PASMCs. Resting [Ca(2+)](i) was 96 +/- 4 nmol/l. PE (10 micromol/l) stimulated oscillations in [Ca(2+)](i), with a peak amplitude of 437 +/- 22 nmol/l and a frequency of 1.01 +/- 0.12/min. Thapsigargin (1 micromol/l) was used to deplete sarcoplasmic reticulum (SR) Ca(2+) after extracellular Ca(2+) was removed. Under these conditions, a nifedipine-insensitive, sustained increase in [Ca(2+)](i) (140 +/- 7% of control value) was observed when the extracellular Ca(2+) concentration was restored; i.e., capacitative Ca(2+) entry was demonstrated. Capacitative Ca(2+) entry also refilled SR Ca(2+) stores. Capacitative Ca(2+) entry was attenuated (32 +/- 3% of control value) by 50 micromol/l of SKF-96365 (a nonselective Ca(2+)-channel inhibitor). Tyrosine kinase inhibition with tyrphostin 23 (100 micromol/l) and genistein (100 micromol/l) also inhibited capacitative Ca(2+) entry to 63 +/- 12 and 85 +/- 4% of control values, respectively. SKF-96365 (30 micromol/l) attenuated both the amplitude (15 +/- 7% of control value) and frequency (50 +/- 21% of control value) of PE-induced Ca(2+) oscillations. SKF-96365 (50 micromol/l) abolished the oscillations. Tyrphostin 23 (100 micromol/l) also inhibited the amplitude (17 +/- 7% of control value) and frequency (45 +/- 9% of control value) of the oscillations. Genistein (30 micromol/l) had similar effects. Both SKF-96365 and tyrphostin 23 attenuated PE-induced contraction in isolated pulmonary arterial rings. These results demonstrate that capacitative Ca(2+) entry is present and capable of refilling SR Ca(2+) stores in canine PASMCs and may be involved in regulating PE-induced Ca(2+) oscillations. A tyrosine kinase is involved in the signal transduction pathway for alpha(1)-adrenoreceptor activation in PASMCs.

Adrenergic alpha-Agonists↗
PubMed2002

Role of Ca2+ signaling in the regulation of endothelial permeability.

The vascular endothelial cell forms a semipermeable barrier between blood and interstitium. Inflammatory mediators such as thrombin and histamine induce vascular leakage defined as increased endothelial permeability to plasma proteins and other solutes. Increased endothelial permeability is the hallmark of inflammatory vascular edema. Inflammatory mediators that bind to heptahelical G protein-coupled receptors (GPCR) trigger increased endothelial permeability by increasing the intracellular Ca(2+) concentration ([Ca(2+)](i)). The rise in [Ca(2+)](i) activates key signaling pathways, which mediate cytoskeletal reorganization (through myosin light chain (MLC)-dependent contraction) and disassembly of VE-cadherin at the adherens junctions. The Ca(2+)-dependent protein kinase C (PKC) isoform, PKC-alpha, plays a critical role in initiating endothelial cell contraction and disassembly of VE-cadherin junctions. The increase in [Ca(2+)](i) induced by a variety of agonists is achieved by the generation of inositol 1,4,5-trisphosphate (IP3), activation of IP3 receptors (IP3R), release of stored intracellular Ca(2+), and Ca(2+) entry through plasma membrane channels. Recent findings demonstrate that IP3-sensitive Ca(2+) store depletion activates plasma membrane cation channels (i.e., store-operated cation channels (SOC) or Ca(2+) release activated channels) to cause Ca(2+) influx in endothelial cells. This mode of Ca(2+) influx is also known as capacitative Ca(2+) entry (CCE). Store-operated Ca(2+) influx signals increase in permeability and nitric oxide (NO) production and provokes changes in gene expression in endothelial cells. Recent studies have established that the Drosophila transient receptor potential (TRP) gene family of channels expressed in endothelial cells can function as SOC. Deletion of one of the TRP homologues, TRPC4, in mouse caused impairment in store-operated Ca(2+) current and Ca(2+) store release activated Ca(2+) influx in aortic and lung endothelial cells (LEC). In TRPC4 knockout (TRPC4(-/-)) mice, acetylcholine-induced endothelium-dependent smooth muscle relaxation was drastically reduced. In addition, TRPC4(-/-) mice LEC exhibited lack of actin stress fiber formation and cell retraction in response to thrombin activation of proteinase-activated receptor-1 (PAR-1) in endothelial cells. The increase in lung microvascular permeability in response to thrombin receptor activation was inhibited in TRPC4(-/-) mice. These results indicate that endothelial TRP channels such as TRPC1 and TRPC4 play an important role in signaling the increase in endothelial permeability.

Animals↗
PubMed2000

In vivo venodilator action of fenoldopam, a dopamine D(1)-receptor agonist.

The effects of the dopamine D(1)-receptor agonist fenoldopam were compared with those of the D(2)-receptor agonist R(-)-propylnorapomorphine and vehicle on mean arterial pressure (MAP), mean circulatory filling pressure (MCFP, the driving force of venous return), arterial resistance (R(a)), venous resistance (R(v)), heart rate (HR) and cardiac output (CO) in groups of thiobutabarbitone-anaesthetized rats pre-treated with i.v. injection of mecamylamine (3.7 micromol kg(-1)) and continuously infused with noradrenaline (6.8 nmol kg(-1) min(-1)). The vehicle did not alter any haemodynamic variables. All doses of fenoldopam (0.5, 2 and 16 microgram kg(-1) min(-1)) reduced MAP, R(a) and R(v), and increased CO. At the highest dose, fenoldopam also increased HR and reduced MCFP. All doses of R(-)-propylnorapomorphine (0.5, 2 and 16 microgram kg(-1) min(-1)) increased MAP but did not significantly alter CO, R(v) and MCFP. Both R(a) and HR were increased by the highest dose of R(-)-propylnorapomorphine. Our results indicate that fenoldopam reduces MAP and MCFP, and markedly increases CO through reductions of arterial and venous resistances. The effects of fenoldopam in dilating arterial resistance and capacitance vessels were similar. In contrast, R(-)-propylnorapomorphine elevates MAP through an increase in arterial resistance but has minimal effects on CO, MCFP and venous resistance. Both drugs have a small direct, positive chronotropic action at the highest dose.

Animals↗
PubMedDate not supplied

[The linking of the basic functions of the cerebral vessels under the influence of adrenergic substances and general anesthetic agents].

In chronic experiments on conscious and quiet rats norepinephrine, isoproterenol, ether, hexenal and ketamine narcosis decreased the cerebral fraction of cardiac output but increased transcapillary filtration in tissues of rubidium chloride and blood supply in the capacitive part of blood vessels. The changes produced by pyroxan, obsidan and ornid in the same conditions were insignificant. A decrease of the cerebral fraction of cardiac output, an increase of transcapillary filtration of rubidium in the brain tissues and regional blood supply took place under the action of pyroxan, obsidan and ornid in experiments with immobilization of rats.

Anesthetics↗
PubMed1994

Analysis of flow in coronary epicardial arterial tree and intramyocardial circulation.

A mathematical model combining the coronary flow in the epicardial arterial tree and the intramyocardial circulation is presented. The epicardial arterial tree is represented by a resistive capacitive network based on its realistic anatomy. The intramyocardial flow is affected by the pump action of the contracting myocardium through the extravascular compressive pressure (ECP), which, in turn, affects the dynamic resistance and compliance changes based on the relationship between the transmural pressure and the cross-sectional area of a vessel. The model accounts for the autoregulatory mechanism of the intramyocardial compartments (arteriolar, microvascular and venular) and is structured according to the epicardial coronary anatomy. Realistic coronary epicardial arterial flow patterns are obtained, which compare well to experimentally measured data in six dogs under basal conditions and during reactive hyperemic response. Simulations of the average transmural flow in the three intramyocardial vascular compartments show that the flow in the arterial side is predominantly diastolic, with a systolic retrograde component, and is dominantly systolic antegrade flow in the venular side, consistent with experimental data. Interestingly, the transmurally average microcirculatory flow is continuous, with very small change throughout the cardiac cycle, and is practically insensitive to changes in the model parameters. The model presents a quantitative tool that describes the dynamic patterns of coronary flow in relationship to muscular and extravascular parameters.

Animals↗
PubMed1994

Venoconstriction of hepatic capacitance vessels during hemorrhage in cats: efferent mechanisms.

Cats anesthetized with pentobarbital sodium were hemorrhaged (1 ml.min-1.kg body wt-1) until arterial pressure declined to 55 mmHg. Hepatic volume was recorded by plethysmography. In controls, 20 +/- 5 (SD) ml/kg was removed and hepatic volume decreased 3.6 +/- 0.8 ml/kg. Splanchnic nerve section or administration of hexamethonium-atropine reduced hemorrhage volumes (to 10.3 +/- 2.3 and 4.8 +/- 1.8 ml/kg, respectively) and liver volume changes (to 1.5 +/- 0.5 and 0.7 +/- 0.3 ml/kg, respectively). Section of only the hepatic nerves had no effect on hemorrhage volume or the decrease in hepatic volume. Section of the hepatic nerves after removal of the adrenals and kidneys also had no significant effect on hemorrhage volume or the decrease in liver volume. We conclude that the hepatic capacitance response to hemorrhage does not require direct sympathetic venoconstriction of the hepatic capacitance vessels. Changes in inferior vena caval pressure play a significant but small role. The splanchnic nerves (excluding hepatic nerves) play a major role, possibly by splanchnic arteriolar constriction. Whereas the liver comprises only 2.5% of the body weight, it contributed 18% of the hemorrhage volume.

Adrenalectomy↗
PubMed1984

[Effect of plant glycosides on resistance and capacitance vessels].

In the anaesthetized cat, SCOA ( Miroton ), a product which contains extracts from Scilla , Convallaria , Oleander and Adonis , displays not only its well-known positive inotropic effect but has also constrictor effects on veins when applied in intravenous doses of 21.5-100 GPU /kg ( GPU = guinea-pig units, i.e. cardiotoxic equivalents related to 1 g body weight of guinea-pigs). The latter effect differs in that it is somewhat more prolonged. With intraduodenal administration the doses required to achieve equal peak effects as with intravenous injection are about 4 times larger and this suggests a relatively good enteral availability in the cat. SCOA constricts not only veins but also arteries. However, this latter effect is comparatively small and occurs only after intraarterial infusion of high doses (9.1 and 91 GPU /min, respectively).--The cardiac glycosides contained in the drug product primarily account for its vasoactive qualities. The venous constrictor effect correlates with the guinea-pig units. In qualitative respects, the pure glycosides cymarin , convallatoxin , proscillaridin , and scillaren exert equal effects. There is, however, evidence that the correlation between the effect on veins and on the heart differs for the glycosides tested. Based on equal guinea-pig units, the adonis extract, for instance, acts on capacitance vessels about twice as much as scilla , oleander and convallaria extracts. Cymarin , too, has a stronger effect on veins than would be expected from its cardiotoxic effect. The action on arteries and veins are based on different mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1999

Evidence for a contribution of store-operated Ca2+ channels to NO-mediated endothelium-dependent relaxation of guinea-pig aorta in response to a Ca2+ ionophore, A23187.

A23187 (6S-[6alpha,8beta,9beta,11alpha]-5-(methylamino) -2-[[3,9,11-trimethyl-8-[1-methyl-2-oxo-2-(1H-pyrrol-2-yl)ethyl]-1,7- dioxaspiro[5.5]undec-2-yl]methyl]-4-benzoxazolecarboxylic acid, calcimycin), an antibiotic Ca2+ ionophore, produces an endothelium-dependent vascular relaxation. In the present study, pharmacological features were functionally characterized of endothelium-dependent relaxant response of guinea-pig aorta to A23187, especially focusing on the possible Ca2+ source and Ca2+ mobilization mechanisms in endothelial cells responsible for the vasorelaxant response to the Ca2+ ionophore. A23187-induced endothelium-dependent relaxation was suppressed profoundly by N(G)-nitro-L-arginine (L-NNA; 3 x 10(-4) M) or calmidazolium (3 x 10(-5) M), suggesting that nitric oxide (NO) produced by the enhanced activation of Ca2+/calmodulin-dependent endothelial NO synthase (eNOS) is largely responsible for the relaxant response of this artery to A23187. In the Ca2+-free solution without EGTA, NO-mediated endothelium-dependent relaxation induced by A23187 was almost abolished, which suggests that Ca2+ entry from extracellular space into endothelial cells plays the key role in the A23187-induced functional vasorelaxation. On the other hand, SK&F96365 (1-[beta-[3-(4-methoxyphenyl)propoxy]-4-methoxyphenethyl]-1H-imidazole; 5 x 10(-5) M) and Ni2+ (3 x 10(-4) M), both of which inhibit capacitative Ca2+ influx through store-operated Ca2+ channels (SOCCs), attenuated significantly NO-mediated endothelium-dependent relaxation by A23187. Furthermore, A23187-induced endothelium-dependent relaxation was suppressed more strongly than endothelium-independent relaxation induced by SIN-1 (3-morpholino-sydnonimine), an NO donor, when aortic preparation was preconstricted with high KCl instead of agonistic stimulation (prostaglandin F2alpha). These findings suggest that NO-mediated endothelium-dependent relaxant response of guinea-pig aorta to A23187 is preceded by the increase in endothelial cytosolic free Ca2+ concentration ([Ca2+]cyt) due to the enhanced Ca2+ influx from extracellular space. In the enhanced Ca2+ entry leading to the stimulation of eNOS and NO-mediated functional relaxant response of guinea-pig aorta to A23187, activation of SOCCs but not the Ca2+ entry through plasma membrane Ca2+-specific routes made by A23187 seems to play the predominant role. It is most likely that A23187 acts primarily at the Ca2+ store sites in endothelial cells, which subsequently depletes stored Ca2+ to activate SOCCs via unidentified mechanisms.

Animals↗
PubMed1994

Inhibition of capacitative Ca2+ entry by a Cl- channel blocker in human endothelial cells.

We have used the patch clamp technique in combination with intracellular calcium measurements to measure simultaneously Ca2+ entry and ionic currents activated by emptying of intracellular Ca2+ stores (capacitative Ca2+ entry and Ca2+ release-activated Ca2+ currents, CRAC) in human endothelial cells from umbilical veins. Intracellular stores were depleted of Ca2+ by preincubating endothelial cells for 20 minutes with 2 microM thapsigargin in Ca(2+)-free solution. Reapplication of 10 mM [Ca2+]e evoked an increase in [Ca2+]i indicating Ca2+ influx after the thapsigargin-induced store depletion (capacitative Ca2+ entry), however no measurable CRAC could be detected. The increase in [Ca2+]i after [Ca2+]e resubmission was substantially reduced in the presence of 50 microM NPPB (5-nitro-2-(3-phenylpropylamino)-benzoic acid) from 0.77 +/- 0.25 microM to 0.2 +/- 0.06 microM (n = 6) at a holding potential of -40 mV. Estimates of the capacitative Ca2+ entry at various membrane potentials from the first time derivative of the Ca2+ transients showed a highly inwardly rectifying I-V curve with a Ca2+ inward current amplitude of 1.0 +/- 0.3 pA (membrane capacitance 59 +/- 9 pF, n = 8) at -80 mV. This current amplitude was decreased to 0.32 +/- 0.12 pA (n = 6) in the presence of 50 microM NPPB. This corresponds to a decrease in the Ca2+ permeability of the endothelial cell membrane from 0.15 x 10(-8) cm/s (control) to 0.06 x 10(-8) cm/s (50 microM NPPB).

Calcium↗
PubMedDate not supplied

Reflex activation in allergen-induced nasal mucosal vascular reactions.

Subjects with allergic rhinitis were challenged unilaterally with diluent and increasing doses of allergen. Challenge with the highest dose of allergen was also carried out after topical anesthesia of the nasal cavity using lidocaine. In the contralateral, unprovoked nasal cavity the mucosal blood flow was determined using the 133Xenon wash-out technique and the nasal airway resistance was determined by rhinomanometry before and after challenge. Nasal symptom scores were estimated 15 min after each challenge. Blood flow in the nasal mucosa in the unprovoked right nasal cavity decreased in a dose-dependent manner for th two highest doses of allergen where a reduction of 21% (p less than 0.05) and 26% (p less than 0.01) was obtained. Nasal airway resistance increased somewhat after the highest dose (p greater than 0.05). Topical anesthesia in the provoked nasal cavity inhibited the decrease in blood flow in the unchallenged nasal cavity. These findings suggest that the changes in the tone of the resistance vessels, but not the capacitance vessels, which are induced by allergen, are largely reflex-mediated.

Adult↗
PubMed1997

Delayed autoregulation of the Ca2+ signals resulting from capacitative Ca2+ entry in bovine pulmonary artery endothelial cells.

1. In calf pulmonary artery endothelial (CPAE) cells loaded with fura-2, the effects of ATP on Ca2+ entry were mediated entirely by the ability of P2U purinoceptors to stimulate InsP3 formation, empty intracellular Ca2+ stores and thereby activate capacitative Ca2+ entry. 2. Restoration of extracellular Ca2+ to cells with empty intracellular stores evoked transient increases in cytosolic [Ca2+] ([Ca2+]i) which then declined to an elevated plateau. These overshoots in [Ca2+]i were not a consequence of store refilling nor of desensitization of the capacitative pathway. Similar responses were recorded from cells in which Ca2+ uptake into mitochondria had been inhibited by microinjection of Ruthenium Red. The amplitudes of the capacitative Ca2+ signals decreased at lower extracellular [Ca2+], but [Ca2+]i invariably overshot before slowly declining to an elevated plateau. Even modest increases in [Ca2+]i therefore caused a delayed attenuation of the Ca2+ signal evoked by capacitative Ca2+ entry. 3. Modest pre-elevation of [Ca2+]i inhibited the ability of subsequent capacitative Ca2+ entry to further increase [Ca2+]i. The onset of the inhibition was slow (half-time (t1/2), approximately 100 s) and more tightly correlated with the preceding peak [Ca2+]i than with the [Ca2+]i immediately preceding Ca2+ entry. Recovery was also slow and complete only after [Ca2+]i had returned to its basal level for 320 +/- 3 s. 4. In thapsigargin-treated cells loaded with mag-fura-2, the peak [Ca2+]i that followed restoration of extracellular Ca2+ was accompanied by an abrupt approximately 2.5-fold decrease in the rate of Mn2+ entry, which then continued indefinitely at the reduced rate, demonstrating a rapid partial inactivation of the capacitative pathway. 5. The half-time for Ca2+ removal from the cytosol was significantly slower during the rising (t 1/2 = 22 +/- 2.5 s) than during the falling (t 1/2 = 7.1 +/- 0.7 s) phase of the Ca2+ overshoot evoked by addition of extracellular Ca2+ to thapsigargin-treated cells. 6. We conclude that an increase in [Ca2+]i rapidly inhibits the capacitative pathway and more slowly activates mechanisms that remove Ca2+ from the cytosol. Reversal of either or both of these regulatory mechanisms can occur only a considerable time after [Ca2+]i has been completely restored to its resting level. These mechanisms are likely to protect cells from excessive increases in [Ca2+]i and contribute to oscillatory changes in [Ca2+]i.

Adenosine Triphosphate↗
PubMed1997

Microvascular anatomy of the nose.

The microvasculature of the nose consists of: 1) A dense subepithelial network of capillaries, with fenestrations between the endothelial cells. This network provides nutrients to the epithelium and glands, and allows passage of water into the lumen for evaporation and air-conditioning. 2) A system of capacitance vessels or sinuses, which when they distend, block the nasal lumen, and when they empty, open the nasal passages. Changes in their volume will affect the filtering and air-conditioning functions of the nose. 3) Arteriovenous anastomoses which allow rapid passage of blood through the mucosa. They are probably important in air-conditioning, and in the countercurrent mechanisms that tend to keep the brain cool in a hot dry climate. The anatomical interrelationships between these different systems is not well understood, nor is their differential control in terms of actions of mediators and nerves. In neurogenic inflammation sensory nerves are excited and release local mediators such as substance P via axon reflexes. These sensory neuropeptides will cause vasodilatation, vascular congestion and extravasation of liquid from the postcapillary venules, with resultant oedema and exudate. They may also cause secretion from the submucosal glands.

Arteriovenous Anastomosis↗
PubMed1980

[Construction of the microcirculatory bed of palatine salivary glands of rats].

Owing to multilayer graphic reconstruction, it was possible to state that resistance and capacitance microvessels of the palatal salivary glands are localized within the lamina propria of the palatal mucous membrane. The structural principle of blood transport and distribution is performed by a closed arteriolar system in which separate modules are distinct. In an individual module area there are tightly packed 5--6 glandular lobes, 1 or 2 of them are not connected with the gland which is completely within the limits of the module. The network of the canals delivering and distributing blood among the modules has a concentric-radial form. Every precapillary arteriole, passing in interlobular connective tissue layer towards the center--the collecting vein--delivers blood to two halves of the adjoining lobes. At various levels of organization of the vascular microcirculatory bed in the rat palatal salivary gland, canals with a predominant blood flow are revealed and functional appraisal for each is given. The palatal salivary gland lobe is noted to correspond most fully to our idea of the elementary autonomic secretory unit.

Animals↗
PubMed2002

In the presence of L-NAME SERCA blockade induces endothelium-dependent contraction of mouse aorta through activation of smooth muscle prostaglandin H2/thromboxane A2 receptors.

1. The mechanism of transient contractions induced by the sarcoplasmic-endoplasmic reticulum calcium ATPase (SERCA) blocker cyclopiazonic acid (CPA) in the presence of L-NAME was investigated in mouse aorta. 2. The contractions elicited by 10 micro M CPA required an intact endothelium, were dependent upon external Ca(2+) and were prevented by 10 micro M indomethacin, the inhibitor of prostaglandin synthesis, or 1 micro M SQ29548, the specific prostaglandin H2/thromboxane A2 (PGH2/TXA2) receptor blocker. 3. A blocker of receptor/store operated Ca(2+) channels and voltage gated calcium channels (VGCC), SK&F 96365 (10 micro M), completely abolished the contractions, while a specific blocker of VGCC nifedipine (1 micro M) inhibited them by one third. 4. Dichlorobenzamyl hydrochloride, a blocker of Na(+)/Ca(2+) exchange effectively prevented return of tension to baseline value. 5. At higher concentrations (30-100 micro M) CPA induced indomethacin-resistant tonic contractions of mouse aorta. The CPA dose response curve for tonic contractions is shifted to the right compared to the transient contractions suggesting that smooth muscle is less sensitive to CPA than endothelium. 6. PGH2/TXA2 receptors in mouse aorta are highly sensitive to the thromboxane analogue U46619 (EC(50) : 1.93 nM). This compound stimulates contractions even in the absence of external Ca(2+), which are abolished by the Rho-kinase inhibitor HA-1077. 7. The results suggest that 10 micro M CPA induced capacitive Ca(2+) entry in endothelial cells stimulating the release of PGH2/TXA2, which subsequently caused smooth muscle contraction dependent on Ca(2+) influx and myofilament sensitization by Rho-kinase. Higher concentrations of CPA (30-100 micro M) directly induced contraction of mouse aortic smooth muscle.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1988

Interaction between renin and the autonomic nervous system in hypertension.

The abnormal distribution of plasma renin values described in established essential hypertension are also found in patients with very early, borderline hypertension. In established hypertension, renin values have been used to draw inferences about the pathophysiology of blood pressure elevation. Within this concept, the low-renin state is considered a volume-dependent (volume expanded) form of hypertension. The high-renin state is viewed as high-resistance hypertension caused by a renin-dependent vasoconstriction. However, the pathophysiology of high- and low-renin borderline hypertension does not follow the prediction from the volume-vasoconstriction theory. The high-renin state is often associated with an increase in cardiac output and normal values of vascular resistance. Even when the cardiac output is normal and the total peripheral resistance is elevated in high renin, the vasoconstriction is not renin-angiotensin dependent. The high-renin borderline and mild hypertension is a state of generalized, increased, sympathetic drive to the heart, blood vessels, and kidneys. After the influence of the autonomic nervous system is removed by pharmacologic blockade, blood pressure in patients with high-renin values becomes normal. To the contrary, pharmacologic antagonization of angiotensin II with a converting enzyme inhibitor does not lead to normal blood pressure values in patients with high-renin. Patients with borderline hypertension with low renin have normal plasma and blood volume values. However, because of decreased compliance of the peripheral capacitance space, the blood volume is shifted from the peripheral to the central (cardiopulmonary) portion of the circulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Circulatory response to exercise in health.

Engagement in muscular exercise involves complex local and nervous adjustments of the circulation. In the active muscles, including cardiac muscle, the resistance vessels relax in response to local chemical changes to provide an increase in blood flow adequate for their metabolic requirements. There is increased release of norepinephrine from the sympathetic nerve endings as a result of increased sympathetic outflow; the resultant alpha-receptor activation leads to constriction of both systemic resistance and capacitance vessels outside the active muscles, and the beta-receptor activation leads to an increase in heart rate, shortening of the refractory period, and enhancement of myocardial contractility. As a consequence, the filling pressure of the heart and arterial blood pressure are maintained, and the increase in left ventricular output is directed primarily to the active muscles. During upright exercise, the action of the leg muscle pump contributes to the maintenance of the cardiac filling pressure. As exercise continues and body temperature rises, the skin flow increases to dissipate heat from the body. Static exercise causes a greater increase in arterial blood pressure than dynamic exercise. This is due to the combination of an increase in cardiac output and in total systemic vascular resistance as a consequence of increase sympathetic outflow and mechanical compression of the vessels in the active muscles. The hemodynamic changes result from activation of ergoreceptors in the contracted muscles and from central command. The increase in pressure helps to oppose the mechanical compression. The arterial baroreceptors are reset so that they operate normally around the higher blood pressure.

Adult↗
PubMed1986

The physiology of the nose.

The nose, as an organ initiating reflexes affecting itself and the rest of the body, and as a target organ of control, is highly complex. Its innervation includes parasympathetic, sympathetic, sensory/afferent, and somatic motor nerves, which combine in a variety of morphologic pathways. The vasculature of the nose contains capacitance vessels such as sinusoids and distensible venules, as well as arteriovenous anastomoses, arterioles, capillaries, and venules. The secretory tissue of the nose includes epithelial cells, submucosal glands, and relatively large anterior or lateral serous glands; in addition, some species have specialized secretory glands. The nose is the source of many powerful reflexes, including the diving response, sneeze and sniff reflexes, and reflexes affecting autonomic nervous function to the cardiovascular system, airways in the lungs, the larynx, and other organs. Axon reflex control of the nasal vasculature is also important. The nasal vasculature can be shown to be under parasympathetic and sympathetic control, but there is little precise information concerning the effect of nerves on different types of blood vessels. Pharmacologic experiments show that vascular resistance and vascular volume can be separately influenced by nerves and mediators, and that vascular resistance and airway resistance are not necessarily inversely related. Nasal secretion is also under the influence of both parasympathetic and sympathetic nerves, and can be induced by a wide range of neurotransmitters and mediators. In general, the concentrations needed to promote secretion are considerably higher than those that affect vascular resistance, at least with regard to the lateral nasal gland of the dog. In humans, nasal patency is affected by several nervous inputs, presumably acting via vascular beds. The nasal cycle is the alternation of resistances between the two sides of the nose, on which other changes are superimposed. In exercise and hyperpnea, nasal airflow resistance decreases, presumably with vascular decongestion. Recent studies of the crutch reflex (the ipsilateral nasal congestion caused by stimulation of the axilla) show that some of the reflex inputs to the nose can be unilateral.

Airway Resistance↗