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PubMed1986

Alpha-adrenergic receptors and blood pressure control.

Alpha-adrenergic receptors play an important role in the regulation of blood pressure (BP). There are 2 principal types of alpha receptors, alpha 1 and alpha 2, and both participate in circulatory control. Alpha 1 receptors are the classic postsynaptic alpha receptors and are found on vascular smooth muscle. They determine both arteriolar resistance and venous capacitance, and thus BP. Alpha 2 receptors are found both in the brain and in the periphery. In the brain stem, they modulate sympathetic outflow. Their function in the periphery is not yet fully understood, but they may contribute both to control of sympathetic tone and to local and regional blood flow. Drugs that enhance central alpha 2 activity, such as clonidine, guanfacine and the active metabolite of methyldopa, can significantly lower BP and are effective in the long-term control of hypertension, either alone or in combination with other drugs. While central alpha agonists, as a class, share a common pharmacologic mode of action, side effects, e.g., sedation and drowsiness, occur to different degrees with different drugs, and the individual agents also vary in terms of their propensity for causing withdrawal hypertension. The use of low-dose regimens or of newer drugs, such as guanfacine, with its longer half-life and duration of action, may reduce the likelihood of adverse reactions associated with this class of drugs.

Adrenergic alpha-Agonists↗
PubMed1981

Physiologic basis of vasodilator therapy for heart failure.

In congestive heart failure, an increase in impedance to left ventricular ejection appears to be an important factor in impairing left ventricular performance. Arteriolar narrowing and decreased arterial compliance will decrease the left ventricular ejection fraction, whereas reduction in venous capacitance will shift blood centrally and increase cardiac filling. These vascular events may result from activation of the sympathetic nervous system and the renin-angiotensin system. Vasodilator drugs, by relaxing the increased vascular tone, will reduce ventricular volume and increase stroke volume, and thus improve the patient's hemodynamic and myocardial metabolic state. Translation of this acute hemodynamic response into a therapeutic benefit from long-term therapy is an attractive but not yet entirely proved thesis. Long-term controlled trials must eventually establish the place of vasodilator drug therapy in the management of different types of congestive heart failure. Furthermore, additional insight is needed into the potential for selective therapy that is tailored to counteract specific mechanisms of vasoconstriction in individual patients.

Heart Failure↗
PubMed2003

Signaling of hypoxia-induced autonomous proliferation of endothelial cells.

Endothelial cells exhibit an autonomous proliferative response to hypoxia, independent of paracrine effectors. In cultured endothelial cells of porcine aorta, we analyzed the signaling and compared hypoxia with mitochondrial inhibition by rotenone. Particularly, roles of the mitogen-activated protein kinase (MAPK) kinase (MEK)/MAPK pathway and cytosolic Ca2+ were studied. Hypoxia resulted in increased proliferation by 65+/-2%. Hypoxia induced transient activation of p42 MAPK (phosphorylation rose from 11+/-5 to 51+/-7%), followed by translocation of p42 MAPK into the nucleus. The proliferative response was diminished after inhibition of the MEK/MAPK pathway by PD 98059 (20 microM) or UO 126 (10 microM) but not sensitive to 8-phenyl-theophillin (10 microM), an adenosine receptor blocker, nor to a neutralizing antibody for vascular endothelial growth factor (VEGF). Inhibition of intracellular Ca2+ release, capacitive Ca2+ influx, or removal of extracellular Ca2+ prevented hypoxic Ca2+ overload and the proliferative response. Suppression of cytosolic Ca2+ rise did not interfere with activation of p42 MAPK but abolished its nuclear translocation. Effects of hypoxia were mimicked by rotenone (10 microM. Transient hypoxic inhibition of mitochondria induces a proliferative endothelial response mediated through Ca2+-independent activation and Ca2+-dependent nuclear translocation of p42 MAPK. This proliferative response is independent of adenosine or VEGF.

Active Transport, Cell Nucleus↗
PubMed1978

Forearm hemodynamics and responses to exercise in middle-aged adult-onset diabetic patients.

Much of the difficulty in assessing the progress of diabetic angiopathy and effects of experimental modes of therapy arises from the lack of quick, simple, inexpensive, and noninvasive tests to perform on the circulatory system of human subjects. We report here on values obtained by the use of mercury-in-rubber strain gauge plethysmography on 15 middle-aged, adult-onset diabetics who had minimal clinical evidence of microangiopathy. Standard tests are described for assessing forearm vascular function at rest, during tonic exercise of the fingers, and after interrupted repetitive exercise of the fingers. When matched against a similar aged nondiabetic group, the diabetics had slightly higher forearm vascular resistance at each level of exercise, a marked reduction (approximately 50 per cent) in capillary filtration coefficient, which is believed to be related to vascular filtering surface area, and a slight reduction in venous capacitance at all levels of exercise. The method of mercury-in-rubber strain gauge venous occlusion plethysmography provides the clinician with a sensitive and inexpensive tool with which to follow the evolution of angiopathy in diabetic patients.

Blood Pressure↗
PubMed1988

Effects of calcium antagonists on myogenic and neurogenic control of resistance and capacitance vessels in cat skeletal muscle.

The effects of five different calcium antagonists (diltiazem, felodipine, nifedipine, nimodipine, and verapamil) on cat skeletal muscle resistance and capacitance vessels were studied in a whole organ preparation. These calcium antagonists seemed to have the similar qualitative effects on these vascular functions. Calcium antagonists were found to be potent inhibitors of myogenic vascular reactivity (here defined as the maximal increase in flow resistance evoked by a sudden rise of transmural pressure). Basal vascular tone and vascular tone induced by low frequency stimulation of sympathetic nerves were both less sensitive to these drugs than vascular tone induced by myogenic vascular reactivity. Sympathetically mediated vascular tone at high stimulation frequencies seemed to be least sensitive. Further, resistance vessels were much more sensitive to these drugs than capacitance vessels. Finally, basal tone in the large bore arterioles were more sensitive than in the small bore arterioles, a surprising finding which was interpreted with the aid of computer simulations using a mathematical model of local vascular control in cat skeletal muscle. The model suggested that this difference could be due to a delicate interaction between myogenic vascular reactivity and metabolic vascular control. It is suggested that the inhibition of myogenic vascular reactivity is a factor contributing to the edema formation of calcium antagonists.

Animals↗
PubMedDate not supplied

Comparative investigations of aspirin and indomethacin effects on blood flow in the vascular bed of skeletal muscles at rest and during muscle contractions in dogs and cats.

The effecs of two different inhibitors of prostaglandin synthesis--aspirin and indomethacin--on the blood flow in the vascular bed of the hindleg of vagotomized animals were studied before, during and after muscular activity of this limb. The responses of resistance and capacitance vessels were recorded simultaneously. Muscular contractions were evoked stimulating electrically (4 impulses/second) the peripheral part of the sciatic nerve. It was found that both inhibitors reduced exercise hyperaemia and postexercise hyperaemia. The response of the capacitance vessels was also reduced during muscular contractions. The obtained results confirmed that endogenous prostaglandins participate in the vascular response during exercise in the precapillary and postcapillary sections of microcirculation in the muscles. The particularly important effect of aspirin on postexercise hyperaemia in dogs in relation to cats is stressed.

Animals↗
PubMed1999

Age-related abnormalities in arterial compliance identified by pressure pulse contour analysis: aging and arterial compliance.

The objective of this study was to evaluate age-related changes in pulsatile arterial function. Aging alters arterial pulsatile function and produces consistent changes in the pressure pulse contour. A reduced systemic arterial compliance that can be derived from analysis of the pulse contour is regarded as the best clinical index of impaired pulsatile arterial function and may mark the presence of early vascular damage. We analyzed intra-arterial brachial artery waveforms in 115 healthy normotensive volunteers (83 men, 32 women) and radial artery waveforms obtained with the use of a calibrated tonometer device in 212 healthy volunteers (147 women, 65 men). A computer-based assessment of the diastolic pressure decay and a modified Windkessel model of the circulation were used to quantify changes in arterial waveform morphology in terms of large artery or capacitive compliance, oscillatory or reflective compliance in the small arteries, inertance, and systemic vascular resistance. Large artery compliance and oscillatory compliance correlated negatively with age for both invasive and noninvasive groups (r=-0.50 and r=-0.55; r=-0.37 and r=-0.66; P<0.001 for all). The slopes of the regression lines for the decline in oscillatory compliance with age were significantly steeper than those recorded for large artery compliance estimates. The change in blood pressure with age independently contributed to the decrease in large artery compliance but not oscillatory compliance in both groups. Consistent age-related changes were found in the pressure pulse contour by analysis of waveforms obtained invasively or noninvasively from the upper limb. The change in the oscillatory or reflective compliance estimate was independent of blood pressure change and may represent a better marker than large artery or capacitive compliance of the degenerative aging process in altering pulsatile arterial function.

Adult↗
PubMed1997

Measuring venous capacitance and blood flow in pregnancy.

Forearm or calf venous plethysmography has been used in pregnant women to examine the effects of pregnancy on the vascular system and more recently to measure blood flow changes in response to intra-arterial infusion of vasoactive substances. To examine the assumption that venous capacitance and blood flow measurements are the same in the forearm and calf, venous plethysmography was conducted simultaneously on the forearm and calf in normal (NP) and hypertensive pregnant women (HTP) in their third trimester and in normal nonpregnant women (N). All studies were made on the right forearm and calf with subjects in the left lateral recumbent position. There was no significant difference between venous capacitance in the forearm (median: 124 x 10(3)mL/100mL/mmHg for both NP and HTP) and leg (134 [NP] and 106 [HTP] x 10(3)mL/100mL/mmHg) for both pregnant groups but venous capacitance in the nonpregnant group was greater in the leg than arm (174 versus 112 x 10(3)mL/100mL/mmHg, p < 0.001). Blood flow was similar in the leg and forearm (median 4.9 versus 3.9mL/100mL/min respectively) in nonpregnant women. Forearm blood flow was also similar to calf flow in NP women (6.2 versus 4.3mL/100mL/min respectively) but greater than calf blood flow in HTP (9.7 versus 5.3mL/100mL/min, p < 0.01). Using left lateral recumbency, forearm and calf vein capacitances are similar in pregnant women, in contrast to nonpregnant women. Blood flow is higher in the forearm than the calf only in hypertensive pregnant women. These observations should be borne in mind when interpreting studies of regional blood flow in pregnancy.

Adult↗
PubMed2000

Sustained endothelial nitric-oxide synthase activation requires capacitative Ca2+ entry.

Endothelial nitric-oxide synthase (eNOS), a Ca(2+)/calmodulin-dependent enzyme, is critical for vascular homeostasis. While eNOS is membrane-associated through its N-myristoylation, the significance of membrane association in locating eNOS near sources of Ca(2+) entry is uncertain. To assess the Ca(2+) source required for eNOS activation, chimera containing the full-length eNOS cDNA and HA-tagged aequorin sequence (EHA), and MHA (myristoylation-deficient EHA) were generated and transfected into COS-7 cells. The EHA chimera was primarily targeted to the plasma membrane while MHA was located intracellularly. Both constructs retained enzymatic eNOS activity and aequorin-mediated Ca(2+) sensitivity. The plasma membrane-associated EHA and intracellular MHA were compared in their ability to sense changes in local Ca(2+) concentration, demonstrating preferential sensitivity to Ca(2+) originating from intracellular pools (MHA) or from capacitative Ca(2+) entry (EHA). Measurements of eNOS activation in intact cells revealed that the eNOS enzymatic activity of EHA was more sensitive to Ca(2+) influx via capacitative Ca(2+) entry than intracellular release, whereas MHA eNOS activity was more responsive to intracellular Ca(2+) release. When eNOS activation by CCE was compared with that generated by an equal rise in [Ca(2+)](i) due to the Ca(2+) ionophore ionomycin, a 10-fold greater increase in NO production was found in the former condition. These results demonstrate that EHA and MHA chimera are properly targeted and retain full functions of eNOS and aequorin, and that capacitative Ca(2+) influx is the principle stimulus for sustained activation of eNOS on the plasma membrane in intact cells.

Aequorin↗
PubMed1995

Oxidized glutathione decreases luminal Ca2+ content of the endothelial cell ins(1,4,5)P3-sensitive Ca2+ store.

The model oxidant, t-butyl hydroperoxide (t-buOOH), inhibits Ins(1,4,5)P3-dependent Ca2+ signalling in calf pulmonary artery endothelial cells. Metabolism of t-buOOH within the cytosol is coupled to the oxidation of glutathione. In this study, we investigated whether oxidized glutathione (GSSG) is the intracellular moiety responsible for mediating the effects of t-buOOH on Ca2+ signalling. The increase in cytosolic [Ca2+] stimulated by application of 2,5-di-t-butylhydroquinone (BHQ) was used to estimate the luminal Ca2+ content of the Ins(1,4,5)P3-sensitive store in intact cells. Luminal Ca2+ content was unaffected by t-buOOH (0.4 mM, 0-3 h) unless intracellular GSSG content was concomitantly elevated. The effect was specific for increased GSSG and was not replicated by depletion of GSH. These results suggest that cytosolic GSSG, produced endogenously within the endothelial cell, decreases the luminal Ca2+ content of Ins(1,4,5)P3-sensitive Ca2+ stores. Depletion of internal Ca2+ stores by GSSG may represent a key mechanism by which some forms of oxidant stress inhibit signal transduction in vascular tissue. At the plasma membrane, t-buOOH is known to inhibit the capacitative Ca2+ influx pathway. Increased intracellular GSSG potentiated the inhibitory effect of t-buOOH on Ca2+ influx, thereby providing the first evidence that activity of the capacitative Ca2+ influx channel is sensitive to thiol reagents formed endogenously within the cell.

Animals↗
PubMed1990

Vascular selectivity of felodipine: clinical experience.

Felodipine is a new calcium antagonist with vascular selectivity. It has a high potency in arterial resistance vessels and no apparent action on capacitance vessels. It lacks significant effects on myocardial contractility and cardiac conduction. It is an effective antihypertensive agent and may be safely combined with beta-adrenoceptor blockade. This report outlines work confirming the vascular selectivity of felodipine by examining its clinical effects in hypertension, ischemic heart disease, and congestive heart failure.

Animals↗
PubMed1984

Systemic and pulmonary hemodynamic responses to intracranial hypertension.

Experiments were conducted in anesthetized, vagotomized, and open-chest dogs. Total heart bypass was performed to perfuse the systemic and pulmonary circulations with constant flow. The venous outflows were diverted into reservoirs. We studied the simultaneous changes in systemic vascular resistance (SVR) and capacity (SVC) as well as pulmonary vascular resistance (PVR) and capacity (PVC) during a period of intracranial hypertension (ICH). In 20 dogs with an intracranial pressure of 164 +/- 12 mmHg, SVR increased by 110% and SVC decreased by 8.4 +/- 1.2 ml/kg. The increase in PVR reached 69%, and the decrease in PVC amounted to 1.24 +/- 0.40 ml/kg body wt or 9.7 +/- 3.9 ml/100 g lung wt. The results indicate that ICH exerts profound effects on both systemic and pulmonary resistance and capacitance vessels. An analysis from the pulmonary blood volume change suggested that the pulmonary vascular compliance was significantly reduced by ICH from a control value of 0.33 +/- 0.06 to 0.26 +/- 0.05 ml X mmHg-1 X kg-1. In the pulmonary circulation, an elevation of left atrial pressure with lung volume expansion attenuated the resistance response, while it increased the capacity reduction. When pulmonary blood volume was kept constant by a constant venous outflow equal to the arterial inflow, the response of capacitance vessels to ICH increased both pulmonary arterial and venous pressures associated with a slight change in PVR. These findings suggest that an increase in pulmonary venous pressure with a constant or increased blood volume reduced the ICH-induced change in resistance.

Animals↗
PubMed1995

The effects of elevated compartment pressure on tibial arteriovenous flow and relationship of mechanical and biochemical characteristics of fascia to genesis of chronic anterior compartment syndrome.

PURPOSE: The purpose of this study is to evaluate the effects of increased compartment pressure on anterior tibial arteriovenous flow patterns and to determine whether mechanical and biochemical properties of fascia are responsible for compartment pressure abnormalities. METHODS: Twenty patients with chronic anterior compartment syndrome (CACS) and 20 age-matched control subjects had compartment pressure measurements and analysis of tibial arterial and venous flow before and after fasciectomy. Fascia specimens were evaluated for thickness, stress failure, structural stiffness, and total collagen content and prevalence of collagen cross-linkage. RESULTS: Pressures were significantly elevated in patients with CACS versus control subjects (23.8 mm Hg vs 6 mm Hg). No significant difference in tibial arterial flow could be detected in either group (43 cm/sec mean vs 41.9 cm/sec mean). Venous drainage was severely impaired in patients with CACS but not in control subjects. CACS fascia was thicker and stiffer than control fascia specimens (0.35 mm +/- 0.12 mm, 109 +/- 65 MN/mm; versus 0.22 mm +/- 0.06 mm; 60.3 +/- 22 MN/mm). Fasciectomy normalized postoperative compartment pressures and improved venous drainage. Collagen content per unit mass was similar for both CACS and control fascia specimens, although collagen cross-linking was significantly lower in the CACS fascia than in the controls. CONCLUSIONS: Tibial venous drainage is impaired, but arterial flow is not in patients with CACS. Fascia thickness and structural stiffness can account for increased pressure in CACS compartments. Collagen content and cross-linkage are unrelated to fascia stiffness or thickness. Postoperative improvement in vascular hemodynamics and reduction in compartment pressure is caused by increased capacitance in the compartment after fasciectomy.

Anterior Compartment Syndrome↗
PubMed2004

Vestibular activation does not influence skin sympathetic nerve responses during whole body heating.

The cutaneous vasculature and eccrine sweat glands are modified by both thermal and nonthermal factors. To determine the effect of thermal stress on the vestibulosympathetic reflex, skin sympathetic nerve activity (SSNA) and cutaneous end-organ responses were measured in 10 subjects during static head-down rotation (HDR) and dynamic yaw and pitch (30 cycles/min) to activate the otolith organs and semicircular canals. SSNA (microneurography of peroneal nerve), cutaneous vascular conductance (CVC; laser-Doppler flux/mean arterial pressure), sweat rate (capacitance hygrometry), and body temperature were collected during normothermia and after whole body heating. Body temperature was controlled by perfusing neutral (34-35 degrees C) or warm (44-46 degrees C) water through a tube-lined suit. During normothermia, HDR did not alter SSNA (-0.4 +/- 4.4% change), CVC (4.2 +/- 6.9% change), or sweat rate (-2.7 +/- 1.2% change) within the innervated area of skin. Dynamic yaw and pitch also did not elicit significant changes in SSNA, CVC, or sweat rate during normothermia. Whole body heating significantly increased internal temperature (0.8 +/- 0.1 degrees C), mean skin temperature (4.1 +/- 0.2 degrees C), CVC (322 +/- 109% control), and sweat rate (0.35 +/- 0.08 mg.cm(-2).min(-1)). After whole body heating, HDR did not significantly alter SSNA (3.2 +/- 7.6% change), CVC (-7.3 +/- 3.9% change), or sweat rate (-3.3 +/- 1.9% change). Dynamic yaw and pitch also did not produce significant changes in SSNA, CVC, or sweat rate after whole body heating. These data suggest that vestibular activation by head movements is not a nonthermal factor affecting SSNA and cutaneous end-organ responses in humans.

Adult↗
PubMed2002

[Clinical features of neurohumoral regulation of the vascular tonus in patients with recurrent nasal bleedings].

Norepinephrine (NE), dopamine, histamine and serotonin levels in the blood were measured fluorometrically in 54 patients with nasal bleedings (NB) aged 15 to 23 years. Of them, 18 patients suffered from habitual NB, 36 had NB because of hypertension. Biogenic amines were studied before and after graded exercise (GE). Low basal levels of serotonin, NE and dopamine were found in all the examinees. Patients with habitual NB had also high basal level of histamine. Such correlation of biogenic amines points to abnormal relations between vasoconstrictive and vasodilating mechanisms of neurohumoral vascular regulation disturbing microcirculation in nasal mucosa, suppresses tonicity of the capacitive vessels, leads to their overfilling, progression of circulatory hypoxia and metabolic acidosis, makes bleedings recurrent. Similarity of neurohumoral adaptation reactions to GE in patients with habitual and hypertensive NB suggests the presence of the same mechanisms of NB onset and their recurrences in various primary causes.

Dopamine↗
PubMed2005

Evidence against reciprocal regulation of Ca2+ entry by vasopressin in A7r5 rat aortic smooth-muscle cells.

Recent studies by Moneer and Taylor [(2002) Biochem. J. 362, 13-21] have proposed a reciprocal regulation of two Ca2+-entry pathways by AVP ([Arg8]-vasopressin) in A7r5 vascular smooth-amuscle cells. Their model proposes that AVP inhibits CCE (capacitative Ca2+ entry) and predicts a rebound of CCE after the removal of AVP. In the present study, we used whole-cell perforated patch-clamp techniques to measure ISOC (store-operated current) corresponding to CCE in A7r5 cells. When 100 nM AVP is present, it activates ISOC with no apparent rebound on removal of AVP. ISOC activated by thapsigargin or cyclopiazonic acid was not inhibited by 100 nM AVP. We also used fura 2 fluorescence techniques to re-examine the model of Moneer and Taylor, specifically focusing on the proposed inhibition of CCE by AVP. We find that 100 nM AVP activates capacitative Mn2+ entry and does not inhibit thapsigargin- or cyclopiazonic acid-activated Mn2+ entry. Moreover, Ca2+ entry after depletion of intracellular Ca2+ stores is enhanced by AVP and we detect no rebound of Ca2+ or Mn2+ entry after AVP removal. On the basis of these findings, we conclude that AVP does not inhibit CCE in A7r5 cells.

Animals↗
PubMed2002

[Aldosterone and cardiovascular diseases, more than water and salt retention].

The activation of the different neurohumoral system plays an important role in the different mechanisms of the development and progression of arterial hypertension and chronic heart failure. The renin-angiotensin II-aldosterone system is one of the key players in this process. With the use of ACE-inhibitors in the treatment of hypertension and heart failure, less attention has been paid to aldosterone. Aldosterone has been only considered as a humoral factor playing a role in salt and water homeostasis and as a consequence controlling arterial blood pressure. There is now evidence of vascular synthesis of aldosterone besides the secretion at the adrenal cortex as well that aldosterone is involved in the development of left ventricular hypertrophy in arterial hypertension, decreased arterial elasticity of the large arteries in chronic heart failure and is inversely correlated with venous capacitance in chronic heart failure. Moreover aldosterone plays a role in the disturbances of the vascular matrix, endothelial dysfunction as well as baroreflex dysfunction. This work has contributed indirectly in the unraveling of the mechanisms which could be partly explained the results of the RALES-trial. The new research project will be focused on the study of the cross-talk between the autonomic nervous system and aldosterone in normotension, arterial hypertension and heart failure.

Aldosterone↗
PubMed1985

[Resistance, capacitance and exchange functions of the vessels of the small intestine in acute hypothermia].

Shifts of vascular functions occurred in two phases in cats cooled from 37 degrees C to 25 degrees C: first, a considerable increase of the integral vascular pre- and postcapillary resistance as well as of the capillary hydrostatic pressure with obvious reduction of the capillary filtration coefficient (CFC) and stretching ability of the venous bed occurred at 31-29 degrees C in the organ under study; the second phase (25 degrees C) involved a decrease of the integral vascular pre- and postcapillary resistance, a considerable augmentation of venous vessels stretching ability and stabilizing of the CFC at the level reached at 31 degrees C. Experiments with decentralized intestine revealed no virtual differences of the vascular function shifts in hypothermia whereas the values of integral resistance of the intestine's vascular bed, precapillary resistance, capillary pressure and of the venous vessels stretching ability were considerably decreased.

Animals↗