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Biomedical subjects

A L Mark

Publications and source records attributed to A L Mark.

At least 109 records · Page 6Linked to original sources
PubMed1988

Potentiation of sympathetic nerve responses to hypoxia in borderline hypertensive subjects.

We tested the hypothesis that sympathetic nerve responses to stimulation of chemoreceptors by hypoxia are exaggerated in borderline hypertensive humans. We compared responses to isocapnic hypoxia in eight borderline hypertensive subjects and eight normotensive control subjects matched for age, sex, weight, and height without a family history of hypertension. Measurements of heart rate, mean blood pressure, minute ventilation, and sympathetic nerve activity to muscle were made before and during hypoxia. We also measured responses to a period of voluntary apnea during hypoxia. There were no significant differences between the increases in heart rate, blood pressure, and ventilation in response to hypoxia in the two groups. However, during hypoxia sympathetic activity in the hypertensive subjects increased by 40.6 +/- 13.6% (mean +/- SE), greater than the increase of 20.4 +/- 5.0% in the control subjects (p less than 0.05). In six hypertensive and six control subjects, when apnea was performed during hypoxia, sympathetic activity increased by 605.0 +/- 294.3% in the hypertensive subjects and by only 52.8 +/- 17.3% in the control subjects (p less than 0.001). We conclude that the chemoreceptor reflex is enhanced in borderline hypertensive subjects and results in exaggerated increases in sympathetic nerve activity during hypoxia. This enhanced chemoreceptor reflex is especially obvious when the inhibitory influence of breathing and thoracic afferent activity is eliminated by apnea. This exaggerated response may contribute to excess sympathetic activity in borderline hypertensive subjects and to adverse consequences of sleep apnea in hypertensive subjects.

Apnea↗
PubMed1988

Contrasting reflex effects of chemosensitive and mechanosensitive vagal afferents.

Previous studies have identified two distinct types of cardiac vagal afferents, mechanosensitive and chemosensitive. We tested the hypothesis that these two types of vagal afferents mediate different reflex sympathetic nerve responses. We compared effects of stimulation of chemosensitive and mechanosensitive vagal afferents on renal and adrenal sympathetic nerve activity in rats. In anesthetized, sinoaortic baroreceptor-denervated rats, we measured arterial pressure, heart rate, and renal and adrenal sympathetic nerve activity during intrapericardial administration of phenyl diguanide as a stimulus for chemosensitive afferents and during volume expansion and acute occlusion of the ascending aorta as stimuli for mechanosensitive afferents. Stimulation of chemosensitive afferents with phenyl diguanide (3, 10, and 30 micrograms/kg intrapericardially) caused decreases in renal sympathetic nerve activity (-36 +/- 5, -52 +/- 11, and -71 +/- 5%; p less than 0.01) and in arterial pressure and heart rate but increased adrenal sympathetic nerve activity (+14 +/- 27, +63 +/- 21, and +83 +/- 28%; p less than 0.05). These responses were abolished by vagotomy. Intrapericardial injection of saline vehicle did not change renal and adrenal sympathetic nerve activity. In contrast to the effects of phenyl diguanide, activation of mechanosensitive afferents by volume expansion with intravenous infusion of 6% dextran in 0.9% saline (Dextran 75) decreased both renal and adrenal sympathetic nerve activity. Stimulation of mechanosensitive afferents by acute occlusion of the ascending aorta also decreased both renal and adrenal sympathetic nerve activity. These results indicate that chemosensitive and mechanosensitive cardiac vagal afferents produce different reflex responses: Chemosensitive afferents increase and mechanosensitive afferents decrease adrenal sympathetic outflow.

Adrenal Glands↗
PubMed1988

Epinephrine facilitates neurogenic vasoconstriction in humans.

Numerous studies have suggested that epinephrine may facilitate neural release of NE. There have been no studies in humans that demonstrate the functional significance of this action. To determine whether epinephrine facilitates neurogenic vasoconstriction in humans, we contrasted forearm vasoconstrictor responses to a reflex stimulus (lower body negative pressure [LBNP]) and to intraarterial NE before, during, and 30 min after infusion of epinephrine (50 ng/min) or isoproterenol (10 or 25 ng/min) into a brachial artery. These doses had no systemic effects. We reasoned that if prejunctional stimulation of beta receptors by epinephrine and isoproterenol had functional significance, the vasoconstrictor response to LBNP would be potentiated in comparison to the response to NE (postjunctional mechanism). Studies were done on 23 normal male volunteers. Forearm blood flow was measured with a strain gauge plethysmograph and intraarterial pressure was recorded. The ratio of vasoconstrictor responses to LBNP/NE was used as an index of neural release of the neurotransmitter NE. This ratio increased during infusions of both epinephrine and isoproterenol. 30 min after epinephrine the vasoconstrictor response to LBNP (n = 15) was augmented from +9.9 +/- 2.2 (SE) resistance units (RU) before epinephrine to +16.4 +/- 3.2 RU (P less than 0.05); whereas the response to NE (n = 8) tended to decrease from +8.8 +/- 3.1 RU before to +4.2 +/- 1.2 RU after epinephrine (P greater than 0.05). In contrast, 30 min after isoproterenol the vasoconstrictor responses to LBNP and NE were the same as before isoproterenol. The augmented ratio of responses to LBNP/NE after epinephrine and not after isoproterenol supports the concept that epinephrine, but not isoproterenol, is taken up by the adrenergic terminal, is released subsequently during reflex stimulation, and augments the release of the neurotransmitter NE. These experiments provide the first hemodynamic evidence in humans that epinephrine and isoproterenol facilitate neurogenic vasoconstriction. The sustained effect of epinephrine in contrast to isoproterenol suggests that the late facilitation by epinephrine is related to its neural uptake and subsequent release.

Adult↗
PubMed1988

Sympathetic activation by hypoxia and hypercapnia--implications for sleep apnea.

In normal humans, both hypoxia and hypercapnia result in sympathetic nerve activation, and when combined, i.e. hypoxic hypercapnia, synergistically increase sympathetic activity. Apnea during the hypoxic and hypercapnic stress results in further increases in sympathetic activity. Borderline hypertensive humans have exaggerated sympathetic nerve responses to hypoxia. Hypertensives are also prone to sleep apnea. We suggest that sleep apnea may result in very high levels of sympathetic activity which may contribute to daytime hypertension and/or precipitate cardiovascular catastrophe in hypertensive people during sleep.

Animals↗
PubMed1987

Modulation of cardiovascular reflexes by arginine vasopressin.

Arginine vasopressin (AVP), a potent vasoconstrictor, does not raise arterial pressure in normal humans or neurally intact animals, even during infusions that achieve pathophysiological plasma concentrations. It has been proposed that this is because AVP facilitates the baroreflex control of the circulation. We performed a series of investigations to test this hypothesis, and to determine sites at which AVP might act to augment the baroreflex. In anesthetized rabbits, vasopressin (36 pmol.kg-1.min-1) increased discharge from both medullated and nonmedullated single fibres from aortic baroreceptor nerves during elevations in aortic arch pressure. Similarly, vasopressin (36 pmol.kg-1.min-1) increased the response of left ventricular mechanoreceptor single fibre discharge to elevations of left ventricular end-diastolic pressure. These observations suggest that sensitization of high and low pressure baroreceptors is one mechanism by which vasopressin may facilitate baroreflexes. In a further series of experiments in sinoaortic denervated anesthetized rabbits, vasopressin (18 pmol.kg-1.min-1) facilitated vagally mediated reflex inhibition of renal sympathetic nerve activity during volume expansion. In humans, AVP (0.37 pmol.kg-1.min-1) raised plasma AVP to an antidiuretic level (22 +/- 4 fmol/mL), but did not change blood pressure or the baroreflex control of heart rate or forearm vascular resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Primary resetting of left atrial sensory endings in Dahl salt-sensitive rats fed a low-salt diet.

Vagal afferent pathways contribute to vasomotor inhibition and renal sodium handling by modulating sympathetic nerve activity in rats. Low pressure or cardiopulmonary baroreflex inhibition of sympathetic nerve activity is attenuated in normotensive Dahl salt-sensitive (S) rats fed a low-salt diet. The aim of the study was to record activity in single-fiber vagal filaments from left atrial endings in Dahl S and resistant (R) rats to evaluate the mechanism for the attenuated low pressure baroreflex. Rats were fed a low-salt diet (0.1% NaCl) for 5-7 wk. Seven Dahl R and six S rats were anesthetized with urethan, and catheters were placed in the aorta and left atrium. Single-fiber recordings were obtained from the right cervical vagus. The relationship between left atrial pressure and receptor discharge was obtained during graded aortic snaring. Mean threshold for increased activation of the vagal afferents during volume expansion was 10.4 +/- 0.6 mmHg (means +/- SE) in S and 6.0 +/- 0.4 mmHg in R rats (P less than 0.002). Pressure-discharge curves were significantly shifted to the right in S rats. Maximal sensitivity of the endings expressed as delta discharge/delta LAP was not significantly different in R vs. S, but the right shift in threshold reduced the discharge of endings over a physiological range of filling pressures. We also measured left ventricular end-diastolic pressure (LVEDP) in conscious S and R rats to determine if the resetting of left atrial sensory endings could be explained by elevated left heart filling pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

In search of afferent pathways of a cardiogenic hypertensive chemoreflex.

Injection of serotonin (5-HT) into the left atrium or ventricle activates a hypertensive chemoreflex. The primary purpose of our study was to determine the afferent pathway(s) that mediates this response. A secondary goal was to localize the receptive sites of this reflex. We measured changes in arterial pressure, reflex vascular responses in skeletal muscle and paw, and changes in renal nerve traffic that occurred after the left atrial or left ventricular injection of 5-HT. Injection of 5-HT (100 to 600 micrograms) into left atrium or ventricle produced large reflex increases in vascular resistance and sympathetic outflow. These responses were not reduced after bilateral cervical vagotomy. In separate experiments, increases in renal nerve traffic with left ventricular injection of 5-HT were assessed before and after cardiac sympathetic deafferentation. Interruption of cardiac sympathetic afferent pathways did not significantly attenuate increases in renal nerve activity with 5-HT. Injection of 5-HT (300 micrograms) into the aortic root produced large increases in arterial pressure but this was not observed after injections into the vertebral or common carotid arteries or descending aorta. Injection of 5-HT (100 micrograms) into the left main coronary artery (perfused via a Gregg cannula from an external reservoir) resulted in a depressor reflex (Bezold-Jarisch). In contrast, injection of 5-HT (200 micrograms) into the left ventricle when the drug was prevented from reaching the left coronary artery produced a large pressor response.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗
PubMed1987

Sensitization of aortic baroreceptors by high salt diet in Dahl salt-resistant rats.

High salt diet alters neural cardiovascular control. This influence has been attributed to central neural or efferent mechanisms. To test the hypothesis that a high salt diet might alter afferent baroreceptor function, Dahl salt-resistant (DR) and salt-sensitive rats (DS) were fed a high or a low salt diet. Blood pressure was measured intra-arterially in unanesthetized animals. Aortic baroreceptor function was then evaluated during urethane anesthesia by recording multifiber aortic depressor nerve activity during a phenylephrine-induced blood pressure ramp. Mean arterial pressure in the conscious state was elevated (155 +/- 5 [SE]mm Hg) in DS fed a high salt diet but was normal in DS fed a low salt diet and in DR. Slopes of linear regressions relating aortic nerve discharge to mean arterial pressure were 71% higher in DR fed a high salt diet than in DR fed a low salt diet (p less than 0.025), indicating that high salt potentiated baroreceptor function in DR. In contrast, high salt diet produced no significant effects on baroreceptor function in DS. No salt-induced changes in dynamic or static aortic distensibility (assessed from pressure-volume curves of the in situ isolated arch) were detectable in either rat strain. Absence of salt-induced baroreceptor sensitization in DS was not due to the hypertensive state because the sensitization also failed to occur in separate groups of DS in which salt-induced hypertension had been prevented by chemical sympathectomy with 6-OH-dopamine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Inhibition of muscle sympathetic nerve activity in humans by arginine vasopressin.

Arginine vasopressin, a potent vasoconstrictor, does not raise arterial pressure in normal humans even at pathophysiological plasma levels. To examine whether the pressor effect of vasopressin in humans is buffered by baroreceptor reflex inhibition of sympathetic nerve activity, we recorded postganglionic muscle sympathetic nerve activity directly from the peroneal nerve in 12 normal men before, during, and after a 20-minute intravenous infusion of vasopressin, 4 ng/kg/min, that increased mean plasma concentrations from 6.2 +/- 0.6 to 320 +/- 68 (SE) pg/ml. During the first 5 minutes (n = 8), mean arterial pressure increased from 91 +/- 3 to 97 +/- 4 mm Hg (p less than 0.05) and integrated sympathetic nerve activity decreased from 271 +/- 45 to 156 +/- 33 units (p less than 0.05). At 15 minutes (n = 12), arterial pressure did not differ from control values whereas forearm vascular resistance fell (p less than 0.05) and central venous pressure and heart rate increased (p less than 0.05). Sympathetic nerve activity remained below control levels throughout the infusion (202 +/- 31 vs 254 +/- 40 units before infusion; p less than 0.05). An effect of vasopressin on ganglionic transmission was excluded, since the sympathoexcitatory response to apnea was not attenuated during vasopressin. Thus, pathophysiologic levels of vasopressin in humans cause inhibition of muscle sympathetic nerve activity that is not due to a ganglionic blocking action. The sympathoinhibition may be caused in part by the modest increases in mean arterial and central venous pressures and attendant stimulation of arterial and cardiac baroreceptors. The reflex decrease in sympathetic nerve activity would be expected to buffer the direct vasoconstrictor effects of vasopressin.

Adult↗
PubMed1987

Effects of the cold pressor test on muscle sympathetic nerve activity in humans.

The purpose of this study was to determine the effects of the cold pressor test on sympathetic outflow with direct measurements of nerve traffic in conscious humans and to test the strength of correlation between sympathetic nerve discharge and the changes in arterial pressure, heart rate, and plasma norepinephrine. In 25 healthy subjects, arterial pressure, heart rate, and muscle sympathetic nerve activity were measured with microelectrodes inserted percutaneously into a peroneal muscle nerve fascicle in the leg during immersion of the hand in ice water for 2 minutes. Arterial pressure rose steadily during the first and second minutes of the cold pressor test. Muscle sympathetic activity (burst frequency X amplitude) did not increase in the first 30 seconds of the test but increased from 230 +/- 27 to 386 +/- 52 units (mean +/- SE, p less than 0.05) by the end of the first minute of the test and to 574 +/- 73 (p less than 0.01) during the second minute. In contrast, heart rate increased maximally during the first 30 seconds of the cold pressor test and returned to control during the second minute. The increases in heart rate were abolished by beta-adrenergic blockade. The increases in muscle sympathetic activity during the cold pressor test were correlated with the increases in both mean arterial pressure (r = 0.86, p less than 0.01) and peripheral venous norepinephrine (r = 0.72, p less than 0.05); however, large changes in nerve traffic were associated with small changes in plasma norepinephrine.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1987

Dissociation of sympathetic nerve activity in arm and leg muscle during mental stress.

Mental stress, which increases blood pressure and heart rate, increases forearm blood flow but does not change calf blood flow. The purpose of this study was to determine if mental stress increases muscle sympathetic nerve activity in the leg and causes a dissociation of muscle sympathetic nerve activity in the arm and the leg. We recorded heart rate, blood pressure, and efferent sympathetic nerve activity during mental stress (4 minutes of mental arithmetic) in 13 healthy men. Microelectrodes were inserted percutaneously into a fascicle of the peroneal nerve (leg) and radial nerve (arm) to measure sympathetic discharge to muscle. In Study 1, leg muscle sympathetic nerve activity was recorded in seven subjects. Mental stress significantly increased heart rate and blood pressure. Despite the increased blood pressure (which would be expected reflexly to inhibit sympathetic nerve activity), leg muscle sympathetic nerve activity (in total integrated activity, bursts per 100 heart beats or bursts per minute) increased significantly during stress. Further, whereas heart rate and blood pressure returned to normal during recovery, leg muscle sympathetic nerve activity remained elevated during recovery. In Study 2, simultaneous recordings were made of arm and leg muscle sympathetic nerve activity in six subjects. Mental stress increased heart rate and arterial pressure. Leg muscle sympathetic nerve activity again increased significantly during stress and remained elevated during recovery. In contrast, arm muscle sympathetic nerve activity did not change during stress. However, arm muscle sympathetic nerve activity increased significantly during recovery after stress. These studies indicate that a sympathoexcitatory influence of mental stress overrides or inhibits baroreceptor control of leg sympathetic nerve activity and stress causes a dissociation of arm and leg muscle sympathetic nerve activity with increased outflow to the leg but not to the arm. These observations may contribute to differences in blood flow to arm and leg during mental stress.

Adult↗
PubMed1987

High calcium diet reduces blood pressure in Dahl salt-sensitive rats by neural mechanisms.

We tested the hypothesis that high dietary calcium attenuates hypertension in Dahl salt-sensitive rats by neural as opposed to vascular mechanisms. Four-week-old Dahl salt-sensitive rats were fed a high salt diet (3.3% sodium) with either high (4.0%; n = 21) or normal (0.4%; n = 21) calcium content until they were 10 to 11 weeks old. Total plasma calcium concentration was increased and plasma phosphorus concentration was decreased by the high calcium diet. At 10 weeks, food intake and intestinal absorption of sodium were not altered by the high calcium diet. There were three major observations. First, mean arterial pressure was lower in awake rats fed a high versus normal calcium diet (137 +/- 7, n = 11, vs 165 +/- 6 mm Hg, n = 10, respectively; p less than 0.05). This pressure difference was dependent on intact autonomic transmission, since ganglionic blockade eliminated the significant difference between pressures in rats fed high (78 +/- 5 mm Hg) and normal (85 +/- 6 mm Hg) calcium diets. Second, high calcium intake augmented baroreceptor reflex inhibition of renal sympathetic nerve activity and heart rate during ramp increase in arterial pressure produced by infusion of phenylephrine. Reflex suppression of renal sympathetic nerve activity was twofold greater in rats fed the high (vs normal) calcium diet (-2.79 +/- 0.25 vs -1.34 +/- 0.14% delta/delta mm Hg, respectively; n = 9 rats per group; p less than 0.05). Third, high calcium intake did not attenuate vascular responsiveness, since pressor responses to norepinephrine and angiotensin II did not differ between rats fed high and normal calcium diets after ganglionic blockade.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Dietary treatment of atherosclerosis abolishes hyperresponsiveness to serotonin: implications for vasospasm.

Diet-induced atherosclerosis in primates impairs vasodilator responses and greatly potentiates vasoconstrictor responses to serotonin. Serotonin may play an important role in the pathogenesis of vasospasm. In diet-induced regression of atherosclerosis, intimal lesions are reduced, but maximal vasodilator responses do not improve, perhaps because of vascular fibrosis. Our goal was to determine whether dietary treatment of atherosclerosis reverses the augmented vasoconstrictor responses to serotonin and thus might reduce susceptibility to vasospasm. Normal cynomolgus monkeys, atherosclerotic monkeys, and atherosclerotic monkeys that were given a normal (regression) diet for 18 months were studied. Morphometric studies indicated that the regression diet reduced lesions in the iliac and femoral artery since intimal area was reduced by about 50%. In the hind limb perfused at constant flow, residual resistance during maximal vasodilatation produced by infusion of adenosine tended to be greater in atherosclerotic monkeys than in normals and failed to improve in regression monkeys. In contrast, vasoconstrictor responses to serotonin were greatly potentiated in atherosclerotic monkeys and were restored to normal in regression monkeys. Serotonin (20 micrograms i.a.) decreased hind limb resistance (in mm Hg/ml/min) 0.34 +/- 0.06 (mean +/- SE) in normal monkeys, increased resistance 0.58 +/- 0.17 in atherosclerotic monkeys (p less than 0.05 vs. normal), and decreased resistance 0.70 +/- 0.15 in regression monkeys (p less than 0.05 vs. atherosclerotic). Thus, dietary treatment of atherosclerosis abolishes augmented vasoconstrictor responses to serotonin. It is proposed that treatment of atherosclerosis may be beneficial, even when vasodilator responses fail to improve, by reducing susceptibility to serotonin-induced vasospasm.

Animals↗
PubMed1987

Differential control of heart rate and sympathetic nerve activity during dynamic exercise. Insight from intraneural recordings in humans.

We used microelectrode recordings of muscle sympathetic nerve activity (MSNA) from the peroneal nerve in the leg during arm exercise in conscious humans to test the concept that central command and muscle afferent reflexes produce mass sympathetic discharge at the onset of exercise. Nonischemic rhythmic handgrip and mild arm cycling produced graded increases in heart rate and arterial pressure but did not increase MSNA, whereas ischemic handgrip and moderate arm cycling dramatically increased MSNA. There was a slow onset and offset of the MSNA responses, which suggested metaboreceptor mediation. When forearm ischemia was continued after ischemic handgrip, MSNA remained elevated (muscle chemoreflex stimulation) but heart rate returned to control (elimination of central command). The major new conclusions are that: the onset of dynamic exercise does not produce mass, uniform sympathetic discharge in humans, and muscle chemoreflexes and central command appear to produce differential effects on sympathetic and parasympathetic responses.

Adolescent↗
PubMed1987

Atrial pacing and thallium 201 scintigraphy: combined use for diagnosis of coronary artery disease.

To evaluate the presence of coronary artery disease (CAD), atrial pacing and thallium 201 scintigraphy were performed in 36 patients with stable angina pectoris who were unable to perform an adequate exercise stress test. All patients underwent cardiac catheterization. Nine patients had previously undergone coronary artery bypass surgery. Significant CAD (one or more lesions greater than or equal to 50%) was present in 33 patients. Atrial pacing produced ischemic ST segment depression (greater than or equal to 1 mm) in 18 (55%) patients with CAD, and angina in 20 patients (61%). As the number of vessels with CAD increased, there was no significant change in the sensitivities of pacing-induced angina or ST segment depression for detecting CAD. In the 3 patients without CAD, ST segment depression occurred in 1 patient and angina in none. Thallium 201 scintigraphy demonstrated perfusion defects in 27 (82%) patients with CAD, with fixed defects seen in 13 studies (39%) and reversible defects in 15 (45%). In the 3 patients without CAD, no perfusion defects were seen. The thallium 201 scan successfully predicted the presence of CAD in patients with single-vessel disease but usually underestimated the number of vessels involved in patients with multivessel disease. Combined sensitivity of pacing-induced ST segment depression and an abnormal thallium 201 scan finding for detecting CAD was 91%. The authors conclude that combined atrial pacing and thallium 201 scintigraphy is a useful test for detecting CAD in patients unable to perform an adequate exercise stress test.

Aged↗
PubMed1987

Sensitization of cardiac vagal afferent reflexes at the sensory receptor level: an overview.

The gain or sensitivity of reflexes originating in cardiac sensory receptors with vagal afferent pathways is highly dynamic. This modulation is usually attributed to central nervous system or efferent mechanisms. This paper briefly reviews evidence that modulation of reflexes originating in the heart can also occur at the sensory or afferent level. Five examples are cited: calcium antagonists, cardiac glycosides, arginine vasopressin, atrial natriuretic peptides, and changes in dietary sodium. These examples emphasize the role of ionic and humoral factors in regulation of cardiac vagal afferent function. This concept of sensory modulation of cardiac vagal afferents has implications for cardiovascular pharmacology and for pathophysiological states such as heart failure and hypertension.

Animals↗
PubMed1987

Cardiac sensory receptors in Dahl salt-resistant and salt-sensitive rats.

The Dahl strain of genetically salt-resistant (DR) and salt-sensitive (DS) rats affords an opportunity to explore mechanisms responsible for salt resistance and sensitivity. Dahl sensitive rats exhibit abnormalities in sympathetic neural control of the circulation and in renal sodium handling. Since cardiac baroreflexes participate in regulation of sympathetic nerve activity and sodium excretion, we have evaluated cardiac baroreflex function in DR and DS rats. This article briefly reviews evidence that cardiac sensory endings with vagal afferents are reset to a higher threshold in DS rats before elevation of arterial or cardiac filling pressures, as a result of this resetting, cardiac baroreflex inhibition of sympathetic nerve activity during volume expansion is impaired in prehypertensive DS rats, a high-sodium diet enhances the gain of cardiac baroreflex inhibition of sympathetic nerve activity in DR but not DS rats, and atrial natriuretic factor stimulates cardiac sensory receptors with vagal afferents. Taken together, these studies prompt speculation that humoral factors released during intake of a high-sodium diet may sensitize cardiac baroreflexes and thereby protect against sodium retention and hypertension. An absence of this compensatory adjustment or plasticity in cardiac baroreflex function in DS rats may predispose to salt-induced hypertension.

Animals↗