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PubMed1995

Vascular compliance and mean circulatory filling pressure in trout: effects of ACE inhibition.

Mean circulatory filling pressure (MCFP), whole body vascular compliance (C), and unstressed blood volume (USV) are important indexes of cardiovascular function in mammals, but they have not been measured in fish. In the present experiments, dorsal aortic (PDA) and sinus venosus (PSV) pressures were measured in unanesthetized trout before and during electrical cardiac fibrillation, while blood volume (BV) was manipulated between 50 and 150% of normal. Measurements were repeated after angiotensin-converting enzyme (ACE) inhibition with lisinopril. Cardiac fibrillation (zero-flow condition) rapidly (approximately 5 s) dropped PDA and increased PSV (equals MCFP). MCFP in normovolemic trout (4.8 +/- 0.3 mmHg) varied directly with BV. C determined from in vivo capacitance curves was similar to that obtained gravimetrically, in vitro (3.4 and 3.5 ml.mmHg-1.kg body wt-1, respectively). USV was 13.3 ml/kg body wt (approximately 45% of BV). ACE inhibition reduced PDA in unfibrillated trout at all BV and reduced PDA in fibrillated fish at BV > or = 80%. ACE inhibition did not affect PSV, MCFP, C, or USV. The systemic arteriovenous pressure gradient at zero flow (delta PF0) was greatest at 100% BV (8.2 +/- 0.5 mmHg) and was reduced by ACE inhibition at 80-120% BV. These results show that key indexes of venous function are readily measured in fish and that the trout venous system is not an effector of angiotensin-mediated regulation of arterial blood pressure. Thus angiotensin acts solely on arterial resistance vessels. Furthermore, the drop in delta PF0 during ACE inhibition is due to a decrease in arteriolar resistance.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1995

Additive effects of obesity and hypertension to limit venous volume.

The presence of reduced venous distensibility in obesity might have important hemodynamic effects and could indirectly implicate a role for metabolic factors in vascular control, because loading conditions are different in arterial and in venous vessels. Forearm blood flow and venous volume were measured plethysmographically in 58 subjects, including lean and obese hypertensives and normotensives. Venous volume at 30 mmHg (VV30) was decreased by both obesity and hypertension. This coincided with evidence for better preservation of central blood and stroke volumes with upright posture in obese than in lean subjects. Furthermore, obese hypertensives had lower VV30 than either lean hypertensives or obese normotensives. Postischemic forearm vascular resistance, a surrogate marker for structural luminal cross-sectional area, percent body fat, and fasting insulin each correlated independently with VV30 (P < 0.05) in multivariate analysis. Because nonesterified fatty acid levels are elevated in obese hypertensives and may have potent vascular effects, dorsal hand vein responses to coinfusion of Intralipid 10% and heparin to raise fatty acids locally were obtained in normal volunteers. The local infusion of Intralipid with heparin reduced hand vein distensibility, whereas dextrose and heparin did not (11 +/- 3% vs. 0 +/- 2%, respectively, P < 0.01). This study indicates that obesity and mild hypertension each reduce venous distensibility and that the coexistence of both conditions produces an even greater impairment in venous capacitance. The reduced venous distensibility in obesity appears to reflect structural as well as functional factors and to have systemic hemodynamic effects.

Adult↗
PubMed1988

Serotoninergic mechanisms in hypertension. Focus on the effects of ketanserin.

Aggregating platelets release serotonin, which induces contraction of most vascular smooth muscle by activation of S2-serotoninergic receptors. Serotonin released in the circulation may contribute to the increase in peripheral resistance of hypertension as the responsiveness of blood vessels from hypertensive animals and humans to the vasoconstrictor action of the monoamine is augmented. The data obtained with the new antihypertensive agent ketanserin may favor that interpretation. Ketanserin is a selective S2-serotoninergic antagonist with additional alpha 1-adrenergic blocking properties. In humans, it has a terminal half-life of 12 to 25 hours and is eliminated predominantly by the liver. The hemodynamic profile of ketanserin is that of a vasodilator drug with actions on both resistance and capacitance vessels. On short-term intravenous administration, it lowers blood pressure in hypertensive patients with minimal reflex changes in cardiovascular function. When given orally long term to hypertensive patients, ketanserin causes a sustained reduction in arterial blood pressure, comparable to that obtained with either beta-adrenergic blockers or diuretics. Several studies have shown a greater efficacy in older (greater than 60 years of age) than in younger patients independent of starting pressure. Side effects mainly consist of dizziness, somnolence, and dry mouth, but they are usually not severe. The mechanism underlying the antihypertensive effect of ketanserin is unclear. It cannot be attributed to either S2-serotoninergic or alpha 1-adrenergic blockade alone, but an interaction between the two effects appears to be required.

Humans↗
PubMed2005

Effects of aldosterone on forearm vasculature in treated chronic heart failure.

The nongenomic effects of aldosterone in disease states associated with endothelial dysfunction may differ from those in healthy subjects. The effects of locally infused aldosterone on the forearm blood flow and volume were studied in optimally treated patients with chronic heart failure (CHF). At baseline and after incremental intrabrachial aldosterone, forearm blood flow was assessed using conventional strain gauge plethysmography, and forearm venous volume was assessed by radionuclide plethysmography. Constriction of the resistance vasculature of the forearm without significant effect on forearm venous capacitance was demonstrated in response to aldosterone in patients treated for CHF.

Aged↗
PubMed2001

Deleterious effects of nifedipine on smooth muscle cells implies alterations of intracellular calcium signaling.

Nifedipine (NIF), a calcium channel blocker (CCB) from the first generation of dihydropyridines, induces detrimental effects on patients with cardiovascular diseases. We designed experiments to study, at cellular and molecular level, the mechanisms involved in the induction of deleterious effects by this drug. To this purpose, cultured human smooth muscle cells (HSMC) were used. The effect of NIF and two other CCB (FEL, AML) and inhibitors of intracellular signaling pathways (RR, TG, CAF and GEN) on intracellular calcium [Ca(2+)]I was determined by spectrofluorimetry using Fura 2 AM assay. The results showed that: (i) 10 microM NIF induced the increase of [Ca(2+)]I above the basal values (202.77 +/- 23.98 nM vs. 48.68 +/- 6.45 nM), an effect that was prevented by RR (50.45 +/- 13.9 nM) and was not induced by the two other CCB; (ii) NIF had a thapsigargin-like effect, because it induced the same release of intracellular calcium as TG (212.1 +/- 25.62 nM); (iii) The response to NIF was reduced by 40% after the inhibition of IP3 receptor (121.21 +/- 26.01 nM) and by 50% after the inhibition of tyrosine kinase (101.91 +/- 7.76 nM). Together, these data demonstrate that NIF produces a deregulation of intracellular calcium homeostasis. The abnormal increase of [Ca(2+)]I is due to the activation of store operated channels from the plasma membrane responsible for capacitative calcium entry, a process modulated by the activity of tyrosine kinase and the Ca(2+)-ATPase pump from the sarcoplasmic reticulum.

Amlodipine↗
PubMedDate not supplied

Effects of vasoactive intestinal polypeptide on resistance and capacitance vessels in the nasal mucosa.

Vasoactive intestinal polypeptide (VIP) immunoreactive nerves have previously been demonstrated in the feline nasal mucosa. In the present investigation it is shown that VIP given close arterially dilates both resistance and capacitance vessels in the nose of the cat. This vasodilatation is atropine resistant. It is suggested that VIP serves a physiological role in the neurogenic control of blood vessels in the nasal mucosa.

Animals↗
PubMedDate not supplied

Venodynamic and hemorheological variables in patients with diabetes mellitus.

BACKGROUND: The association between diabetes mellitus and the occurrence of peripheral vascular disease has been well established. However, it is unclear whether the venous circulation is also affected. This study was done to determine whether there is impairment of venous function in the legs of patients with diabetes mellitus and the relationship with rheological parameters. METHODS: Venous occlusion plethysmography was used to assess venous circulation in the legs of 54 diabetic patients at the University Hospital of the West Indies. The venodynamic variables measured were segmental venous capacitance (SVC), maximum venous outflow (MVO), and venous emptying time (VET) at the calf, ankle and great-toe. Plasma fibrinogen concentration (PFC), relative plasma viscosity (RPV) and whole blood viscosity (WBV) were measured by standard techniques. RESULTS: Calf SVC was significantly less in neuropathic diabetic patients (ND) than in non-diabetic subjects (C) (p <0.05). MVO at the calf of ND and non-neuropathic diabetic patients (NND) was significantly lower than in C (p <0.05). VET at the ankle and calf were significantly shorter in ND compared with NND (p <0.05). No statistically significant differences in SVC, MVO and VET among the three groups were observed at the great-toe. PFC was significantly higher in diabetic patients than in the control group. No significant differences were detected in WBV at high or low shear rates. CONCLUSIONS: These findings strongly suggest impairment of venous function in the legs of diabetic patients. This impairment of venous function appears to be unrelated to rheological abnormalities.

Adult↗
PubMed2005

[Changes in voltage-dependent calcium channel currents of vascular smooth muscle cells isolated from small mesenteric arteries of simulated weightless rats].

The aim of the present study was to examine the changes in the function of voltage-dependent calcium channels (VDC) of vascular smooth muscle cells (VSMCs) isolated from small mesenteric arteries of rats subjected to 1-week or 4-week simulated weightlessness. The whole-cell recording mode was used to record current densities and Ba(2+) was used as charge carrier. Curves and fitting parameters describing steady-state activation and inactivation characteristics of VDC were thus obtained. The inward currents recorded from the VSMCs of small mesenteric arteries were mainly the Ba(2+) currents through the long-lasting type VDC (L-VDC). Compared with that of the control rats, the L-VDC current density of VSMCs from small mesenteric arteries showed a trend toward a decrease in the rats after 1-week , while a significant decrease was observed in the rats after 4-week simulated weightlessness. However, there were no significant differences in the opening and closing rates of L-VDCs, the position of steady-state activation and inactivation curves, and in the parameters, V(0.5) and k, between either of the two groups and its respective control group. The membrane capacitance and the reversal potential of the VSMCs from the small mesenteric arteries of rats after simulated weightlessness also showed no significant changes. These findings suggest that the decreased function of the L-VDC in hindquarter VSMCs might be one of the electrophysiological mechanisms that mediate the depressed vasoreactivity and atrophic change in hindquarter arteries during adaptation to simulated weightlessness in rats.

Animals↗
PubMed1998

Capacitative Ca2+ entry and the regulation of smooth muscle tone.

In many non-excitable cells, activation of phospholipase C-linked receptors results in a biphasic increase in the cytosolic Ca2+ concentration; an initial transient increase, owing to the release of Ca2+ from the endoplasmic/sarcoplasmic reticulum (ER/SR), is followed by a much smaller but sustained elevation, which often involves capacitative Ca2+ entry, where depletion of Ca2+ within the ER signals the opening of store-operated Ca2+ channels in the plasma membrane. However, in excitable cells such as smooth muscle, the role of capacitative Ca2+ entry is less clear and the main Ca2+ entry mechanisms responsible for sustained cellular activation have been considered to be either voltage-operated or receptor-operated Ca2+ channels. Although store-regulated Ca2+ entry was known to occur following agonist activation of smooth muscle, it was believed to be important only for the re-filling of the depleted SR and not as a source of activator Ca2+ for the contractile mechanisms. Here, Alan Gibson, Ian McFadzean, Pat Wallace and Christopher Wayman review recent evidence that capacitative Ca2+ entry might indeed be important for the regulation of smooth muscle tone, and that it might provide an important for pharmacological intervention.

Animals↗
PubMed1976

Venous pressure and compliance of the peripheral capacitance vessels.

Compliances of the peripheral capacitance vessels decreased gradually in accordance with the increase in pressure of the brachial vein. The relationship between them formed a number of hyperbolic-like curves, the same results as those found in many cases of both normal subjects and patients with congestive heart failure. The decrease of compliance of the peripheral capacitance vessels was not the result of an organic change, but of a functional change of the vessels caused by distention.

Adult↗
PubMed1980

Differential effects of nitroglycerin, trimetazidine, verapamil and SK&F 24260 on venous return as revealed by the open-loop method in the dog.

To obtain detailed information concerning the effects of different vasodilators on venous return, experiments were carried out on 28 dogs by the use of the open-loop method. Blood from the superior and inferior venae cavae was drained at the level of the tricuspid valve into a reservoir, from which blood was pumped into the right atrium at a constant flow rate. Changes in reservoir volume reflected a total blood shift from the experimental dog and indicated changes in venous return. Drugs were administered into the ascending aorta. Nitroglycerin (1-10 micrograms/kg) decreased systemic blood pressure, total peripheral resistance and venous return but scarcely altered heart rate. Trimetazidine (0.3-3 mg/kg) decreased systemic blood pressure, total peripheral resistance, venous return and heart rate. Verapamil (10-100 micrograms/kg) decreased systemic blood pressure, total peripheral resistance and heart rate, and increased venous return. SK&F 24260 (1-10 micrograms/kg) decreased systemic blood pressure, total peripheral resistance and increased venous return. Only high doses (10-30 micrograms/kg) of SK&F 24260 reduced heart rate. Rigorous measurements of systemic output showed that nitroglycerin (10 micrograms/kg), trimetazidine (3 mg/kg), verapamil (100 micrograms/kg), SK&F 24260 ( 10 micrograms/kg) produced no change in this parameter. SK&F 24260 increased venous return even when sino-aortic baroreceptor reflex was eliminated, ruling out reflex venoconstriction as a possible cause of the increased venous return. The results suggest the following: [1] Vasodilators like SK&F 24260 and verapamil increase venous return by decreasing arterial and/or venous resistance. [2] If the effect which increases venous capacitance prevails over the effect which decreases arterial and/or venous resistance, venous return is reduced as is the case of nitroglycerin and trimetazidine.

Animals↗
PubMed2006

Pregnancy-enhanced Ca2+ responses to ATP in uterine artery endothelial cells is due to greater capacitative Ca2+ entry rather than altered receptor coupling.

Uterine artery endothelial cells (UAEC) derived from pregnant (P-UAEC) and nonpregnant (NP-UAEC) ewes retain pregnancy-specific differences in cell signaling as well as vasodilator production through passage 4. In particular, when P- and NP-UAEC are stimulated with ATP over a 2.5 min recording period, they exhibit similar initial transient peaks in the intracellular free Ca(2+) concentration ([Ca(2+)](i)), but the P-UAEC show a heightened sustained phase. In order to establish whether this was due to an altered subclass of purinergic receptor (P2), both the dose dependency of [Ca(2+)](i) responses to ADP and UTP and the profile of purinergic receptor expression are determined in NP- and P-UAEC. Our findings indicate that while several isoforms of P2X and P2Y receptors are present, it is P2Y2 that is responsible for the ATP-induced initial transient peak in both cell types. We also characterized several key components of the ATP-induced Ca(2+) signaling cascade, including the inositol 1,4,5-trisphosphate receptor and G-proteins, but could not confirm any pregnancy-specific variation in the protein expression that correlated with pregnancy-specific differences in prolonged Ca(2+) signaling. We thus investigated whether such a difference may be inherent to the cell itself rather than specific to the purinergic receptor-signaling pathway. Using thapsigargin (Tg), we were able to demonstrate that the initial Tg-sensitive intracellular pool of Ca(2+)is nearly identical with the capacity in both cell types, but the P-UAEC is nonetheless capable of greater capacitative Ca(2+) entry (CCE) than NP-UAEC. Furthermore, CCE induced by Tg could be dramatically inhibited by 2-aminoethoxydiphenyl borate, suggesting a role for store-operated channels in the ATP-induced [Ca(2+)](i) response. We conclude that changes at the level of capacitative entry mechanisms rather than switching of receptor subtype or coupling to phospholipase C underlies pregnancy adaptation of UAEC at the level of Ca(2+)signaling.

Adenosine Triphosphate↗
PubMed1989

[Quantitative assessment of arterial capacitance in human by noninvasive method].

The purpose of this study was to determine the magnitude of arterial capacitance in human by noninvasive method. In 60 patients (Age: 62.1 +/- 13.4 years) without cardiovascular disease first-pass radionuclide angiography was performed using a digital gamma camera to calculate cardiac output and stroke volume (SV). Systolic interval (ts), diastolic interval (td) and arterial blood pressure were measured using ECG, phonocardiography and sphygmomanometer. We assumed a simple model in which all capacitance (C) lumped into one site with a resistance (R) in parallel to the C. C was calculated by the following basic equations. (Formula; see text) arterial diastolic pressure, E: left ventricular external work. Our results showed: 1) Arterial capacitance ranged from 0.38 ml/mmHg to 2.10 ml/mmHg and more than 60% of stroke volume was pooled in the arterial capacitor during systole. 2) Arterial capacitance fell linearly with age (C = 2.37-0.02 x Age, r = -0.680, p less than 0.001). It is concluded that the capacitor played an important role in arterial circulation.

Adult↗
PubMed2006

alpha2-adrenoceptor agonists as nasal decongestants.

Nasal congestion, one of the major disease features of rhinitis, is induced by the filling of venous sinusoids causing mucosal engorgement with resultant obstruction of nasal airflow. The only available drugs that directly target the underlying vascular features driving nasal obstruction are the sympathomimetic alpha-adrenoceptor agonists due to their vasoconstrictor action. However, standard decongestants are nonselective alpha-adrenoceptor agonists, which have the potential for side-effects liabilities such as hypertension, stroke, insomnia and nervousness. In the present study, the effects of nonsubtype selective alpha(2)-adrenoceptor agonists BHT-920 and PGE-6201204 were evaluated in several isolated nasal mucosa contractile bioassays including dog, pig and monkey, and in a real-time tissue contractility assay using isolated pig nasal explants for BHT-920. The decongestant activity of PGE-6201204 was evaluated in vivo in a cat model of experimental congestion. Our results showed that alpha(2)-adrenoceptor agonists (1) contract nasal mucosa of different species, (2) exert a preferential vasoconstrictor effect on the capacitance vessels (veins and sinusoids), and (3) elicit decongestion. In conclusion, a selective alpha(2)-adrenoceptor agonist causing constriction preferentially in the large venous sinusoids and veins of nasal mucosa and producing nasal decongestion is expected to show efficacy in the treatment of nasal congestion without the characteristic arterio-constrictor action of the standard nonselective sympathomimetic decongestants.

Adrenergic alpha-2 Receptor Agonists↗
PubMed1991

The role of peripheral capacitance and resistance vessels in hypotension following hemodialysis.

The arterial pressure (AP) response to hemodialysis was studied with echocardiography and strain gauge plethysmography in 17 patients with end-stage renal disease; mean AP was unchanged in seven (group A) and was reduced by more than 10 mm Hg in 10 patients (group B). Following dialysis, body weight decreased and heart rate increased equally in both groups. Ejection fraction did not change in the two groups. Left ventricular end-diastolic volume fell by 13 +/- 10% in group A and by 24 +/- 16% in group B. Cardiac index (CI) fell in group B, but remained unchanged in group A. Systemic vascular resistance (SVR) did not change in both groups. The change in mean AP before and after dialysis was significantly correlated with that in Cl (r = 0.49, p less than 0.05), but not with that in SVR. Calf venous pressure-volume curves were not different between the two groups before dialysis. Hemodialysis shifted the curve toward the volume axis for group B but not for group A. These results suggest that hypotension following dialysis is mainly due to the fall in cardiac output, in which increases in venous distensibility play an important role.

Blood Volume↗
PubMed1989

[Venous tone of the limbs. Methods and comparison of 2 areas].

The limb venous tone, index of local venous compliance, was studied with mercury strain gauge plethysmography on 28 male normal subjects (40 +/- 17 years, +/- SD) simultaneously on upper and lower limbs. Measurements were done after 20 mn rest in supine position. Venous tone (VT) equals the slope of the pressure-volume curve established by simultaneous recording of the forearm and calf relative volumes for successive steps of pressure lower than or equal to 30 mmHg. Limb venous capacitance was expressed by means of the maximal limb relative volume (V30) reached for a pressure of 30 mmHg applied through cuffs in standardized conditions. The upper limb venous tone was greater than the lower limb venous tone: 24.3 +/- 8.2 mmHg/ml/100 vs 17.5 +/- 7.9 mmHg/ml/100, p = 0.001. V30 was greater in lower limb than in upper limb: 1.5 +/- 0.5 ml/100 vs 1.1 +/- 0.4 ml/100, p = 0.001. In conclusion, it appears that upper and lower limbs venous distensibility and capacitance are different. They are greater in the lower limb in baseline conditions. Thus simultaneous studies of both these limb venous systems seems important for physiological experiments because of their baseline differences.

Adult↗
PubMed1984

Vascular control in the colon and rectum.

Blood flow and its intramural distribution in the large and small intestines 'at rest' appear to be quite similar, but there are some obvious differences in the regulation of the circulation in these two viscera. Autoregulation of blood flow is well developed in most regions of the gut, with the exception of the colon in which total blood flow varies greatly with arterial blood pressure. However, the colonic autoregulatory capacity can be improved by increasing the metabolic demand of the tissue, e.g. by intra-luminal placement of nutrients. Metabolic and myogenic factors seem to be mutually responsible for autoregulatory behaviour in the large intestine. Functional vasodilatation occurs in the large intestine in response to increased metabolism, a reaction which can be evoked for instance by intra-luminal placement of volatile fatty acids. Mechanical stimulation of the mucosa in the proximal colon also elicits a local hyperaemic response which is postulated to be mediated via an intrinsic nervous reflex possibly releasing 5-HT. In the distal colon and the rectum mechanical stimulation evokes a more wide-spread hyperaemia which is reported to be the result of a pelvo -pelvic reflex with vasoactive intestinal polypeptide (VIP) as a possible mediator. Activation of the sympatho-adrenal system causes constriction of the large intestinal resistance and capacitance vessels. Reflex increase in sympathetic activity, as in exercise or haemorrhage, causes a redistribution of flow and a mobilization of blood from the large intestine to other tissues, thereby, in stress situations, promoting the circulation in more vital organs such as the heart and brain. The most distal part of the large intestine, in particular the rectum, seems to have a unique extrinsic vasodilator control via the parasympathetic pelvic nerves. Activation of these nerves elicits a very pronounced and well maintained vasodilator response in the rectum but only a transient one in the distal colon. This neural vasodilator response is little affected by muscarinic blockade and, hence, largely non-cholinergic in nature. VIP is released from the colon and rectum during pelvic nerve stimulation, the rectal output being especially large and well correlated in time to the concomitant vasodilatation. The rectal vessels are very sensitive to VIP, and intra-arterial infusion of this peptide causes a vascular response which closely resembles that of pelvic nerve stimulation. Such evidence indicates that VIP might be the neurotransmitter responsible for the non-cholinergic vasodilatation in the most distal part of the large intestine.

Animals↗