Tone Pressure Research Articles

Sympathetic nerve activity in the skin in relation to vibration-induced white finger.

With a microneurographic method, sympathetic nerve activity in the skin was recorded from median nerve fascicles of six patients with vibration-induced white finger and four age- and gender-matched normal subjects. At an ambient temperature of 15 degrees C the sympathetic nerve activity was greater in the patients than in the normal subjects. The burst activity was increased in all of the subjects during the water immersion test of the contralateral hand, but neither the increase in the mean burst number nor the mean area under the neurogram showed statistically significant group differences. Thus, although vasoconstrictive tone is greater in patients with vibration-induced white finger than in healthy subjects, no support could be found for the hypothesis that increased vascular tone is of prime importance for attacks of white finger in vibration-exposed subjects.

Effects of vasoconstrictor tone on 02 extraction during isoflurane anaesthesia

Effects of vasoconstrictor tone on 02 extraction during isoflurane anaesthesia

Supraspinal origin of abnormal hindquarter vasoconstrictor tone in spontaneously hypertensive rats.

The object of this study was to determine whether the abnormal hindquarter tone in spontaneously hypertensive rats (SHR) is of spinal origin or not. SHR were implanted with a catheter in the left common carotid and an electromagnetic flow probe around the terminal aorta. About three days after implantation, the spinal cord was transected at Th 1 under ether anesthesia. One hour later, when the rat restored consciousness and the arterial pressure recovered partially to a new plateau level which was significantly higher than that in similarly treated normal rats, ganglionic blockade with hexamethonium did not significantly decrease hindquarter (terminal aortic) resistance, calculated as arterial pressure divided by hindquarter flow. It was concluded that there was no appreciable sympathetic vasoconstrictor tone in the hindquarters of SHR after spinal transection and that the origin of the abnormal tone was at the supraspinal level.

Sympathetic vasoconstrictor tone induced by pentobarbital anesthesia in hindquarters of rats.

Hindquarter (terminal aortic) blood flow (HQF) and arterial pressure (AP) were observed in rats with an electromagnetic flow probe implanted around the terminal aorta and an arterial indwelling cannula. Hindquarter peripheral resistance (HQR) was calculated by dividing mean AP by HQF. Under pentobarbital anesthesia, HQR was decreased significantly (p less than 0.001) by ganglionic blockade with hexamethonium bromide (C6). Since C6 does not change HQR significantly without anesthesia, we interpret that pentobarbital anesthesia generated a sympathetic vasoconstrictor tone in hindquarter resistance vessels. This was further substantiated by the observation that the increase in HQR on infusion of vasopressin was obscure under pentobarbital anesthesia: Presumably, the increase was offset by reflex inhibition of the hindquarter tone induced by anesthesia. The generation of hindquarter vasoconstrictor tone by pentobarbital was for the most part ascribable to the baroreceptor reflex to compensate for the depressor effect of this anesthetic, because it was greatly diminished after severance of the buffer nerves.

Coronary vasodilator reserve in ischemic myocardium of the exercising dog.

Previous work has reported that coronary vasodilator reserve may persist in myocardium rendered ischemic by hypoperfusion. This study investigated the presence and extent of residual coronary vasomotor tone in myocardial regions made acutely ischemic by a flow-limiting coronary stenosis during exercise. Studies were done in chronically instrumented dogs undergoing treadmill exercise in the presence of a coronary stenosis that decreased distal left circumflex coronary artery perfusion pressure to approximately 40 mm Hg. Measurements of myocardial blood flow were made with radioactive microspheres during exercise (6.5 km/hr, 6% grade) before and during intracoronary infusion of the potent coronary vasodilator adenosine (40 micrograms/kg/min). Distal coronary perfusion pressure was held equal before and during intracoronary adenosine infusion (43 +/- 5 versus 42 +/- 5 mm Hg) by adjusting the hydraulic coronary occluder. During exercise in the presence of a coronary stenosis, myocardial blood flow (milliliter per minute per gram) was significantly reduced in all layers of the ischemic posterior region compared with the nonischemic anterior region. During intracoronary adenosine infusion, with no change in coronary perfusion pressure, myocardial blood flow was significantly increased compared with preadenosine flows for both the subendocardial layer flow (1.03 +/- 0.74 versus 0.66 +/- 0.50; p less than 0.05) and mean transmural flow (1.54 +/- 0.59 versus 1.16 +/- 0.36; p less than 0.05). In the presence of a coronary stenosis, regional myocardial segment shortening in the ischemic region during exercise fell significantly to 49 +/- 8% of shortening in the absence of a coronary stenosis but improved modestly during adenosine infusion (65 +/- 7 versus 49 +/- 8%; p less than 0.05). These results indicate that adenosine-responsive coronary vasodilator reserve persists during exercise-induced myocardial ischemia and suggest that residual microvascular vasoconstrictor tone may affect the extent of myocardial hypoperfusion occurring consequent to a flow-limiting coronary stenosis.

Modulation of coronary circulation and the cardiac matrix by the renin-angiotensin system

There are short-term and long-term modulations of cardiac function and cardiac composition by the endocrine and paracrine renin-angiotensin system. First, there is an enhancement of coronary vasoconstrictor tone in severe congestive heart failure due to stimulation of this system. Therapeutic interventions that block the RA-system are able to reduce the increased resistance to coronary flow. Second, there is a relationship between the occurrence of arrhythmias and the degree of sympathetic stimulation in congestive heart failure. The renin-angiotensin system may be involved in arrhythmogenesis because of presynaptic modulation of sympathetic neurotransmitter release. However, in the isolated perfused rat heart no class-specific antiarrhythmic properties could be found for ACE inhibitors during progressive myocardial ischaemia. Third, proliferation of the neointima following injury of a coronary artery is at least in part mediated by angiotensin II. Although ACE inhibition was an effective tool in animal experiments to prevent excessive proliferation of the neointima following ballooning, it was less effective in preventing restenosis in man following a repeat coronary angioplasty. Fourth, preferential proliferation of the cardiac interstitium in experimental hypertension has been associated with activation of the renin-angiotensin system. In patients with essential hypertension ACE inhibitors were not only capable of controlling blood pressure but also of normalizing the previously pathological pattern of diastolic left ventricular filling. In summary, by therapeutic intervention that cause a blockade of this system, cardioprotective and cardioreparative processes can be supported.

Competition between cutaneous active vasoconstriction and active vasodilation during exercise in humans

Cutaneous vasoconstriction occurs in response to the initiation of dynamic exercise in hyperthermia. To find whether this response was due to increased vasoconstrictor activity or to withdrawal of active vasodilator activity, blood flow monitoring with laser-Doppler flowmetry (LDF) was combined with the local iontophoresis of bretylium. Each of six male subjects had two forearm sites treated with bretylium for selective local blockade of noradrenergic vasoconstrictor nerves in skin. LDF was monitored at those sites and at two adjacent untreated sites. Mean arterial pressure (MAP) was measured, and cutaneous vascular conductance (CVC) was calculated as LDF/MAP. After iontophoresis, subjects underwent 3 min of cold stress (water-perfused suits) to verify vasoconstrictor blockade. CVC at untreated sites fell by 35.9 +/- 3.1% (P less than 0.01) and at bretylium-treated sites was not significantly changed (P greater than 0.10). During strenuous exercise in normothermia, CVC at untreated sites fell by 16.1 +/- 4.1% (P less than 0.05) and was unchanged at bretylium-treated sites (+12.7 +/- 6.6%, P greater than 0.05). Whole body heat stress was then applied. When exercise was repeated in hyperthermia, CVC at untreated sites fell by 11.6 +/- 3.8% (P less than 0.05) but was not significantly changed at bretylium-treated sites (+3.6 +/- 3.0%, P greater than 0.30). Following return to normothermia, cold stress verified the persistence of the blockade. We conclude that exercise initiation causes a cutaneous vasoconstriction largely or entirely due to enhanced active vasoconstrictor tone in both normothermia and hyperthermia. Little or no role in this response can be ascribed to reduced active vasodilator activity.

Dynamic regulation of leg vasomotor tone in patients with chronic heart failure

We examined the central hemodynamic (n = 5) and leg blood flow (n = 9) responses to one- and two-leg bicycle exercise in nine ambulatory patients with chronic heart failure due to left ventricular systolic dysfunction (ejection fraction 17 +/- 9%). During peak one- vs. two-leg exercise, leg blood flow (thermodilution) tended to be higher (1.99 +/- 0.91 vs. 1.67 +/- 0.91 l/min, P = 0.07), whereas femoral arteriovenous oxygen difference was lower (13.6 +/- 3.1 vs. 15.0 +/- 2.9 ml/dl, P less than 0.01). Comparison of data from exercise stages matched for single-leg work rate during one- vs. two-leg exercise demonstrated that cardiac output was similar while both oxygen consumption and central arteriovenous oxygen differences were lower, indicating relative improvement in the cardiac output response at a given single-leg work rate during one-leg exercise. This was accompanied by higher leg blood flow (1.56 +/- 0.76 vs. 1.83 +/- 0.72 l/min, P = 0.02) and a tendency for leg vascular resistance to be lower (92 +/- 54 vs. 80 +/- 48 Torr.l-1.min, P = 0.08) without any change in blood lactate. These data indicate that, in patients with chronic heart failure, leg vasomotor tone is dynamically regulated, independent of skeletal muscle metabolism, and is not determined solely by intrinsic abnormalities in skeletal muscle vasodilator capacity. Our results suggest that relative improvements in central cardiac function may lead to a reflex release of skeletal muscle vasoconstrictor tone in this disorder.

Influence of Neuropathy on the Microvascular Response to Local Heating in the Human Diabetic Foot

1. The diabetic neuropathic foot exhibits excess arteriovenous anastomotic shunt flow due to a reduced sympathetic vasoconstrictor tone. Local axon reflexes (mediating postural vasoconstriction, for example) are preserved even in severe diabetic neuropathy. This excess shunt flow and its local neurogenic control may be important in the development of complications of the neuropathic limb. 2. The response of arteriovenous anastomoses to local heating was assessed in 13 diabetic patients with neuropathy (12 insulin-dependent), 10 diabetic control patients (seven insulin-dependent) and 10 normal control subjects. The aim was to study the local reflex control of arteriovenous flow when central sympathetic tone had been largely removed. 3. The change in skin blood flow on local heating to 44 degrees C was measured by using a laser Doppler flowmeter in standard environmental conditions with the foot at heart level. Two sites were assessed: (i) the plantar surface of the great toe (a site in which skin blood flow is dominated by arteriovenous shunt flow) and (ii) the dorsum of the foot (a site without anastomotic flow). 4. It was found that when heat was applied to the plantar surface of the great toe in the diabetic patients with neuropathy a paradoxical decrease in flow through arteriovenous anastomoses occurred, flow declining to 65% (P less than 0.05) of its resting value. This could be compared with an increase in flow over the same time period of 262% and 228% (P less than 0.01) in diabetic control patients and normal subjects, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Sympathetic regulation of cutaneous circulation in the rat

The purpose of the present study was to characterize, in vivo, the function and origin of peripheral α-adrenergic mechanisms in acral regions of the cutaneous microvasculature. Laser-Doppler flowmetry was used to continuously monitor changes in local cutaneous microvascular perfusion (CP) measured at the plantar surface of the terminal phalange in the rat. In ketamine-anesthetized rats, the intravenous administration of phentolamine (a nonselective α-adrenoceptor antagonist) elicited a dose-dependent (0.01–1.0 mg/kg, i.v.) increase in CP, a decrease in mean arterial pressure (MAP) and a marked reduction in cutaneous vascular resistance (CVR). These results demonstrate a high degree of endogenous α-adrenergic tone in the cutaneous microvasculature of the rat. In pithed rats, cutaneous vasoconstriction could be evoked by ganglionic stimulation with DMPP or by electrical stimulation of the peripheral cut end of the sciatic nerve trunk. DMPP and sciatic nerve responses were not altered by propranolol or atropine, but were inhibited by phentolamine. In addition, the effects of DMPP on CP were abolished by bilateral adrenal demedullation, but were unaltered by hindlimb denervation. These results suggest that the predominant vasoconstrictor tone in the cutaneous vasculature is mediated by a humoral action of circulating catecholamines at postjunctional α-adrenoceptors. The adrenal medulla appears to be the origin of this humoral tone. Postganglionic sympathetic nerves play an insignificant role in mediating cutaneous vasoconstriction elicited by ganglionic stimulation.

CARDIOVASCULAR FUNCTIONS OF CENTRAL NORADRENERGIC NEURONS IN RABBITS

1. The cardiovascular actions of central noradrenergic (NA) neurons was examined using the acute neurotransmitter releasing actions of intracisternal 6-hydroxydopamine in conscious rabbits. 2. The predominant actions of NA pathways in the brain-stem are to inhibit vasomotor and cardiac sympathetic activity and to facilitate cardiac vagal responses. 3. NA projections to the spinal cord tonically inhibit vasoconstrictor tone and form part of a high gain control system for responding to changes in specific afferent information. 4. The forebrain NA projections influence heart rate through modulation of the baroreflex gain of the cardiac vagus. 5. Central antihypertensive drugs such as clonidine and alpha-methyldopa mimic most of the brainstem actions of the central NA neurons. They also utilize the ascending NA pathways influencing the baroreflex vagal gain to minimize the baroreflex effects of reducing mean arterial pressure. 6. Thus, NA neurons influence the circulatory system through actions at all levels of the central nervous system and provide a comprehensive framework for integrating cardiovascular information from multiple inputs. This provides a number of targets for future development of useful pharmacological agents.

Baroreflex control of muscle sympathetic nerve activity in borderline hypertension.

Patients with borderline hypertension have exaggerated vascular responses to orthostatic stress produced by tilt or lower body negative pressure (LBNP). It has been suggested that 1) in the supine position, these patients have augmented activity of cardiopulmonary baroreceptors that exerts an increased restraint on sympathetic vasoconstrictor tone; 2) withdrawal of this augmented inhibitory baroreceptor activity during orthostatic stress elicits augmented reflex sympathetic vasoconstrictor outflow; and 3) augmented cardiopulmonary baroreceptor activity may be secondary to impaired arterial baroreflex mechanisms. To test these hypotheses, we recorded muscle sympathetic nerve activity from the peroneal nerve in seven borderline hypertensive subjects and seven age-, sex-, and weight-matched normotensive subjects during three levels of nonhypotensive LBNP and infusions of phenylephrine and nitroprusside. During LBNP, reductions of central venous pressure were similar in borderline hypertensive and normotensive subjects, and arterial pressure and heart rate values were unchanged. Increases of sympathetic nerve activity, however, were significantly greater in borderline hypertensive than in normotensive subjects at each level of LBNP, indicating an augmented gain of the cardiopulmonary baroreflex. To determine whether this augmentation is related to impairment of arterial baroreflexes, we measured changes of sympathetic nerve activity during increases and decreases of arterial pressure produced with infusions of intravenous phenylephrine and nitroprusside. Central venous pressure was held at control levels by LBNP during phenylephrine and saline infusion during nitroprusside. Changes of sympathetic nerve activity during alterations of arterial pressure were similar in borderline hypertensive and normotensive subjects. These data show that cardiopulmonary baroreflex control of SNA is augmented in borderline hypertensive subjects and that this augmentation does not result from an attenuation of the arterial baroreflex.

Beta-adrenergic blockade decreases norepinephrine release in humans

Beta-Adrenergic blockade with propranolol (PRP) has been reported to cause an increase in plasma norepinephrine (NE) levels in humans, which suggests that a reflex increase in sympathetic nervous system (SNS) vasoconstrictor tone compensates for the hypotensive effect of beta-adrenergic blockade. However, plasma NE levels are an indirect measure of SNS activity. We have developed a two-compartment model of NE kinetics to estimate NE release into an extravascular compartment as a more comprehensive measure of systemic SNS activity. To determine whether beta-adrenergic blockade alters extravascular NE release, we studied nine healthy subjects during sequential infusions of saline and PRP. During PRP infusion, there was an increase in plasma NE levels [1.03 +/- 0.13 to 1.27 +/- 0.21 (SE) nM; P = 0.05], but the extravascular NE release rate decreased significantly (15.5 +/- 1.6 to 9.2 +/- 1.2 nmol.min-1.m-2, P = 0.0002). The plasma NE concentration increased despite the fall in extravascular NE release rate primarily because the clearance of NE from plasma declined (1.55 +/- 0.08 to 1.18 +/- 0.07 l.min-1.m-2, P = 0.0001); the NE spillover rate into plasma did not change (1.73 +/- 0.18 to 1.75 +/- 0.23 nmol.min-1.m-2, P = 0.89). We conclude that PRP decreases extravascular NE release in humans. Suppression of SNS activity may be an additional mechanism of action of nonselective beta-adrenergic antagonists in humans.

Participation of both intracellular free Ca 2+ and protein kinase C in tonic vasoconstriction induced by prostaglandin F 2α

The roles of intracellular free Ca 2+ and protein kinase C in the tonic contraction induced by prostaglandin were studied. Prostaglandin F 2α induced tonic contraction of rat thoracic aorta in both control and Ca 2+-free solution. Close correlations were observed between the contractile response of aortic strips and the changes in intracellular free Ca 2+ concentration in vascular smooth muscle cells assessed with the fluorescent Ca 2+ indicator fura 2, both in control and Ca 2+-free solutions. Prostaglandin F 2α also enhanced the production of inositol 1,4,5-triphosphate in vascular smooth muscle cells before the rise of the intracellular free Ca 2+ concentration. Moreover, 1-(5-isoquinoline-sulfonyl)-2-methylpiperazine, an inhibitor of protein kinase C, inhibited the tonic contractions induced by PGF 2α and 12-O-tetradecanoyl phorbol-13-acetate, a direct activator of protein kinase C, at similar concentrations. These results suggest that both intracellular free Ca 2+ and protein kinase C participate in prostaglandin F 2α-induced tonic contraction.

BRL 34915 Ameliorates Oxygen Supply in Ischemic Myocardium by a Simultaneous Enhancement of Coronary Blood Flow and a Reduction of Myocardial function

In the presence of stenotic coronary arteries, oxygen supply in the poststenotic myocardium is reduced. A counterbalancing poststenotic metabolic vasodilatation is attenuated up to 30% by an alpha 2-adrenoceptor-mediated vasoconstrictor tone. In six open-chest dogs, we determined whether cumulative intracoronary doses (1, 4, and 14 micrograms) BRL 34915, a vasodilator with additional dose-dependent cardiodepressant properties, could enhance coronary blood flow and simultaneously reduce myocardial function in poststenotic myocardium, thereby increasing oxygen supply and decreasing oxygen demand. BRL 34915 increased mean left circumflex coronary blood flow [ml/(min.100 g)] dose-dependently from 59 +/- 12.4 (mean +/- SEM) (no BRL) to 227 +/- 43.9 (14 micrograms BRL) (p less than 0.05) in intact coronary arteries and from 36 +/- 7.2 (no BRL) to 74 +/- 13.2 (14 micrograms BRL) (p less than 0.05) distal to a severe stenosis, respectively. In contrast, posterior systolic wall thickening (%), was significantly decreased only by 14 micrograms BRL from 9.7 +/- 1.82 (no BRL) to 7.8 +/- 2.07 (14 micrograms BRL) (p less than 0.05) when coronary arteries were intact and from 8.7 +/- 2.02 (no BRL) to 4.1 +/- 1.39 (14 micrograms BRL) (p less than 0.05) in poststenotic myocardium. We conclude that BRL 34915 can both enhance coronary blood flow in the poststenotic myocardium and decrease myocardial function simultaneously, potentially narrowing the gap between oxygen supply and demand.

Acetylcholinesterase inhibitor, pyridostigmine bromide, reduces skin blood flow in humans

Five subjects exercised on a cycle ergometer for 30 min at 55% peak oxygen consumption on two occasions in an environmental test chamber (ambient temperature = 29 degrees C; dew point temperature = 10 degrees C). Pyridostigmine bromide (PYR), an acetylcholinesterase (AChE) inhibitor, was ingested (30 mg) approximately 150 min before one experiment, and no drug was administered during the other experiment (control). Red blood cell AChE inhibition averaged 40 (+/- 7)% during PYR treatment. Esophageal temperature (Tes), an eight site-derived mean skin temperature, forearm blood flow (FBF; venous occlusion plethysmography), skin blood flow (SkBF; laser-Doppler velocimetry), and metabolic rate (indirect calorimetry) were measured. SkBF decreased 37% after PYR treatment compared with control (P less than or equal to 0.05). The Tes threshold for initiation of cutaneous vasodilation was 36.8 (+/- 0.3) degrees C for the control treatment and 37.0 (+/- 0.3) degrees C for the PYR treatment (P less than or equal to 0.01). FBF was not significantly different between treatments, whereas heart rate was reduced by 7 and 9 beats/min during rest and exercise, respectively (P less than or equal to 0.01). The increased threshold for initiation of cutaneous vasodilation with AChE inhibition by PYR is compatible with nonthermal modulation of the control of thermoregulation through increased acetylcholine (ACh) accumulation. This could potentiate preganglionic transmission to enhance adrenergic vasoconstrictor tone. One suggested mechanism possible at the neuroeffector junction of the sweat gland may be that accumulated ACh diffusion across the adventitia of adjacent arterioles to muscarinic receptors initiates contraction of the smooth muscle.(ABSTRACT TRUNCATED AT 250 WORDS)

Combined effects of autoregulation and vasoconstrictors on hindquarters vascular resistance

Relative contributions of local autoregulatory tone and vasoconstrictor tone to skeletal muscle vascular resistance were studied in anesthetized rats during hypertension produced by vasoconstrictor infusion. Rats were instrumented with a Doppler flow probe on the sacral aorta (SA) to measure blood flow and to allow calculation of vascular resistance. An occluder was placed on the SA and used to produce stepwise reductions in local perfusion pressure. Pressure-flow curves for the hindquarters were obtained in the absence and presence of elevated mean arterial pressure (MAP) produced by infusion of angiotensin II (ANG II; 50-1,247 ng.kg-1.min-1) or phenylephrine (PE; 2.5-12.4 micrograms.kg-1.min-1). Both ANG II and PE infusion increased MAP. For example, MAP was increased by ANG II from 91 to 134 mmHg and by PE from 89 to 156 mmHg. In addition, infusions of ANG II and PE produced dose-dependent rightward shifts in the hindquarters pressure-flow relationship. To examine the effect of pressure on the dose-response relationships of ANG II or PE, local perfusion pressure was adjusted to remain constant at various pressure levels that were independent of MAP during drug infusions. This produced a series of distinct dose-response curves with each curve defined by a different pressure level and with each characterized by a different maximum change in vascular resistance. If local perfusion pressure was not held constant but was permitted to increase with MAP, a compound dose-response curve was obtained in which the combined effects of the change in local pressure (i.e., autoregulation) and vasoconstrictor dose on vascular resistance could be discerned. These data demonstrate that hindquarters blood flow autoregulation continues to occur in the presence of vasoconstrictors. Consequently, autoregulatory mechanisms may be stimulated by any increase in MAP whether associated with systemic vasoconstrictor infusion or activation of neurohumoral pressor systems. The result is an amplified rise in local vascular resistance.

Skin Perfusion Pressure Assessed by Measuring the External Pressure Required To Stop Blood Cell Flux

Laser Doppler flowmetry (LDF) was used to determine the point at which blood flow cessation is achieved under circumferentially applied external counter pressure at the ankle level. In 13 individuals with a normal ankle index, the flow of cessation external pressure (FCEP) was, on average, 28 mmHg lower than the systolic ankle pressure (range: 7-62). In 19 patients with an ankle index below 1.0, FCEP correlated with the ankle pressure (rs = 0.76) and even more closely with the ankle index (rs = 0.82). In patients with a more pronounced degree of arterial occlusive disease, FCEP can be equal to or even higher than the ankle pressure. This may be due to a release of sympathetic vasoconstrictor tone and possibly to the presence of a collateral circulation supplying the skin. Individual LDF values from the skin at rest do not reflect the degree of peripheral circulatory insufficiency.

Cardiovascular responses to carotid sinus baroreceptor stimulation during moderate to severe exercise in man

Our objective was to assess the importance of arterial baroreflexes in maintaining vasoconstriction in active muscle during moderate to severe exercise. Eight subjects exercised for 8-15 min on a cycle ergometer at three levels (averages 94, 194, 261 W) requiring 40-88% of VO2 max. Four times during each exercise level pulsatile negative pressure (-50 mmHg) was applied over the carotid sinuses for 30 s; suction was applied at each ECG R-wave for 250-400 ms. Before and during each neck suction, femoral venous blood flow (FVBF) was measured by constant infusion thermal dilution. At 94 W neck suction significantly reduced blood pressure (BP) (15 mmHg) and heart rate (HR) (7 beats min-1), and raised leg vascular conductance (LVC) (11.4%) without changing FVBF. At 194 W, neck suction reduced BP (9 mmHg), HR (4 beats min-1) and FVBF (5.1%, 240 ml min-1), and raised LVC (5.2%). At 261 W, LVC was unchanged by neck suction, but BP and FVBF both fell (9 mmHg and 650 ml min-1 or 7.4%). We conclude that competing local vasodilation and sympathetic vasoconstriction control muscle blood flow during moderate exercise, and vasoconstrictor tone can be withdrawn by baroreceptor stimulation. High levels of vasoconstrictor outflow to muscle in severe exercise may not originate from baroreflexes.

Cardiogenic reflexes and left ventricular hypertrophy

Studies performed in both animal and human species have shown that receptors anatomically located in the cardiac walls and in the pulmonary vascular bed exert a powerful influence on sympathetic vasoconstrictor tone and renin release from the kidney. This paper will review recent data collected by our group on the effects on this homeostatic reflex function of two different models of cardiac hypertrophy, i.e. that associated with arterial hypertension and that induced by prolonged physical training. It will also examine whether and to what extent cardiopulmonary reflex control of circulation can be restored after an effective antihypertensive pharmacological treatment has induced a regression of the structural alterations of the heart. The results of these studies suggest that cardiopulmonary reflex control of circulation is markedly impaired in the presence of cardiac hypertrophy, with (severe hypertensive subjects) or without (athletes) high blood pressure values. In hypertensives, furthermore, therapeutic regression of cardiac hypertrophy seems to restore, although not fully normalize, this reflex function. Taken together these findings suggest that cardiac hypertrophy, per se, is a condition characterized by the loss of the reflex functions exerted by cardiac receptors, with adverse consequences on cardiovascular homeostasis.