Biomedical subjects

M D Thames

Publications and source records attributed to M D Thames.

At least 55 records · Page 3Linked to original sources

PubMed1989

Effect of chronic myocardial infarction on vagal cardiopulmonary baroreflex.

Sensory endings in the left ventricle are damaged by acute myocardial infarction. The goal of our experiments was to determine whether reflexes that originate in the heart are impaired by chronic myocardial infarction. Inferoposterior (n = 11) or anterior (n = 10) infarction was produced in dogs by ligation and intracoronary injection of rapidly hardening latex into either the proximal left anterior descending or left circumflex coronary arteries. Four weeks after infarction, the changes in renal sympathetic nerve activity induced by phenylephrine infusion, hemorrhage, and volume expansion were assessed before and after sinoaortic baroreceptor denervation. The results in infarct dogs were compared with the results in 11 sham-operated dogs. With arterial baroreceptors intact, baroreflex sensitivity (defined as the percent change in renal nerve activity per millimeter of mercury change in mean pulmonary artery wedge pressure) was similar in all groups of dogs. Following sinoaortic denervation, dogs with anterior and inferoposterior infarction had impaired responses to volume expansion. The responses during hemorrhage were abolished in dogs with inferoposterior infarction. We conclude that chronic myocardial infarction impairs reflexes that originate in the heart in response to changes in cardiac filling pressures.

Animals↗

PubMed1989

Baroreflex control of renal sympathetic nerve activity is preserved in heart failure despite reduced arterial baroreceptor sensitivity.

The purpose of this study was to determine if arterial baroreflex control of sympathetic nerve traffic is impaired in heart failure. We recorded renal nerve activity during changes in arterial pressure while simultaneously recording from aortic baroreceptor afferent fibers in 10 dogs with heart failure induced by rapid ventricular pacing and in 10 sham animals. Sensitivity of the aortic baroreceptors (percent change in nerve activity per millimeters mercury change in mean arterial pressure) was reduced in the heart failure group (heart failure, 2.3 +/- 0.3; sham, 3.6 +/- 0.4, p = 0.02). Despite the reduced sensitivity of aortic baroreceptors in heart failure, there was no difference in the baroreflex gain of renal nerve activity (heart failure, -5.5 +/- 1.4; sham, -5.8 +/- 1.3, p = NS). These values tended to decrease in both groups after vagotomy. The relation between baroreceptor input and renal sympathetic output, or central baroreflex gain (percent change in renal nerve activity divided by percent change in aortic nerve activity) was similar in both groups before vagotomy (heart failure, -2.4 +/- 0.6; sham, -2.3 +/- 0.5, p = NS). Vagotomy reduced central gain in the sham group (-0.9 +/- 0.1, p = 0.03) but not in the heart failure group (-1.7 +/- 0.5, p = NS), suggesting that the contribution of vagal afferents in the baroreflex arc is reduced in heart failure. Baroreflex control of R-R interval was attenuated in heart failure when assessed by blood pressure elevation but not reduction, indicating abnormal parasympathetic but preserved cardiac sympathetic mechanisms in heart failure. Thus, dogs with heart failure exhibit reduced sensitivity of aortic baroreceptors but preserved baroreflex control of renal nerve activity. Reduced baroreceptor sensitivity with preservation of baroreflex control of sympathetic nerve activity may contribute to the sympathoexcitatory state known to exist in heart failure.

Afferent Pathways↗

PubMed1988

Effects of atrial natriuretic factor on urinary concentration of catecholamines and renin secretion in dogs.

This study evaluated the effects of synthetic atrial natriuretic factor (ANF) on renal hemodynamics, urinary excretion of electrolytes, norepinephrine (NE), and dopamine (DA); and renal production of renin in anesthetized dogs. Following a bolus (1 micrograms/kg body weight) and infusion (0.1 microgram/kg/min) for 30 min, there was significant increase in urine flow (220 +/- 41%), glomerular filtration rate (72 +/- 14%), and urinary sodium excretion (170 +/- 34%). There was a decrease in renin secretory rate and the concentration ratio of urine NE to DA following ANF was decreased (p less than 0.05). These data suggest that ANF decreases renal production of NE and renin.

Animals↗

PubMed1988

Atrial natriuretic factor release is enhanced by incremental atrial pacing.

There is ample evidence from animal models indicating that secretion of atrial natriuretic factor (ANF) can be induced by an increase in atrial contraction frequency or atrial distension. The influence of these stimulatory signals on ANF secretion in humans has not been fully elucidated. We assessed the responses to graded right atrial pacing in 28 patients (aged 33 to 70 years) at rates of 100, 125, and 150 beats/min on right atrial pressure, left atrial size (by two-dimensional echocardiography in 9 of 28 patients), and circulating plasma ANF levels. At pacing rates of 125 and 150 beats/min, ANF levels increased from a baseline value of 64 +/- 9 fmol/ml (mean +/- SEM) to 89 +/- 13 fmol/ml (pp less than 0.05) and to 132 +/- 17 fmol/ml, respectively (p less than 0.001). Right atrial pressure increased from a baseline value of 4.1 +/- 0.7 mm Hg to 4.5 +/- 0.6 mm Hg at a pacing rate of 125 beats/min (p less than 0.05) and to 6.1 +/- 0.8 mm Hg at a pacing rate of 150 beats/min (p less than 0.001). Left atrial dimension increased from a baseline value of 44.5 +/- 3 mm to 49.5 +/- 3 mm at a pacing rate of 125 beats/min (p less than 0.05) and increased further to 52.5 +/- 3 mm at a pacing rate of 150 beats/min (p less than 0.001). No significant changes in atrial pressure or size or in plasma ANF were observed at a pacing rate of 100 beats/min.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1988

Effect of transmural versus nontransmural myocardial infarction on inducibility of ventricular arrhythmias during sympathetic stimulation in dogs.

Transmural myocardial infarction interrupts sympathetic nerves and denervates viable muscle distal to myocardial infarction. The effect of sympathetic stimulation on responses to programmed ventricular stimulation was studied in dogs without myocardial infarction (Group I: n = 5), with transmural anterior wall myocardial infarction (Group II: n = 6) and with nontransmural anterior wall myocardial infarction (Group III: n = 9). Ventricular effective refractory period during sympathetic stimulation decreased by 16 +/- 18, 1 +/- 2 and 12 +/- 8 ms (mean +/- SD) in viable muscle of the inferoapical left ventricle in Groups I, II and III, respectively, suggesting efferent sympathetic denervation by transmural myocardial infarction only. Sustained ventricular tachycardia or fibrillation was induced more easily during sympathetic stimulation in six of the six dogs with transmural infarction, but in only two of the nine dogs with nontransmural infarction (p less than 0.01). It is concluded that the partial sympathetic denervation produced by transmural myocardial infarction enhances the ease of induction of ventricular tachycardia and fibrillation during sympathetic stimulation. A similar mechanism may lead to increased risk for lethal arrhythmias during periods of high sympathetic tone in patients with transmural myocardial infarction.

Animals↗

PubMed1988

Isochronal behavior in left ventricular systolic pressure-wall thickness relations.

Regional left ventricular systolic pressure-thickness relations have been used to assess regional load-insensitive contractility with the assumption that they possess linear isochrones that are fundamental to the time-varying elastance model of global pressure-volume relations. We examined the shape and time-varying behavior of pressure-thickness isochrones in six open-chest canine preparations. Transmural wall thickening (sonomicrometry) and ventricular pressure were altered by abrupt preload alterations during control, dobutamine, and propranolol. In all dogs and interventions, linear isochrones (r2 mean +/- SE = 0.91 +/- 0.11) were found at 5-ms intervals. During control, linear isochrone slope rose monotonically from onset to end of systole. Thickness-axis intercepts also varied continuously in time, but peak intercept and maximal slope were asynchronous. Dobutamine caused a steeper earlier maximum slope and increased slope-intercept asynchrony. Propranolol reduced maximum slope and slope-intercept asynchrony. Isochronal data during early systole were better fitted to a parabolic than to the linear model; however, fits to linear and parabolic models were equally good near end of systole. Linear isochronal behavior exists in systolic pressure-thickness relations especially near end systole and is maintained during modest inotropic alterations.

Animals↗

PubMed1988

Reflex effects of prolonged cardiopulmonary baroreceptor unloading in humans.

Most studies of the reflex responses to cardiopulmonary baroreceptor unloading with lower body negative pressure (LBNP) have assessed responses during the first few minutes of LBNP. It is unknown if these early changes are representative of the steady state. Thus we determined the response of heart rate, arterial pressure, forearm vascular resistance (FVR), and plasma norepinephrine (NE), renin (PRA), and aldosterone to prolonged (20 min) LBNP in nine normal subjects. All measurements were obtained at base line and after 3, 10, and 20 min of LBNP (-10, -20, and -40 mmHg). A 20-min recovery period was interposed between each period of LBNP. The heart rate and mean arterial pressure responses to LBNP during all levels of suction were not significantly different at 3, 10, and 20 min of continuous suction. Changes in FVR at 3, 10, and 20 min, respectively, were 18.4 +/- 3.2, 26.3 +/- 4.2, and 19.6 +/- 4.2 U during LBNP -10 mmHg; 33 +/- 7, 30.5 +/- 7.6, and 30 +/- 5.2 U during LBNP -20 mmHg; and 53.6 +/- 11.7, 57 +/- 8.8, and 49.4 +/- 12 during LBNP -40 mmHg, thus indicating a near maximal vasoconstrictor response at 3 min that was sustained throughout the 20 min during all levels of LBNP. Plasma NE rose to near peak level by 3 min. However, PRA and aldosterone changed significantly only after 20 min during LBNP at -10 and -20 mmHg. These data indicate that LBNP activates the sympathetic nervous system early, whereas activation of the renin-angiotensin-aldosterone axis is delayed. Our data should be taken into consideration in the design of future investigations of reflex neurohumoral responses to LBNP.

Adult↗

PubMed1987

Responses of sympathetic nerves to programmed ventricular stimulation.

Ventricular arrhythmias generally result in a decrease in arterial pressure and increases in atrial and ventricular filling pressures which would be expected to induce reflex changes in efferent sympathetic nerve activity to the heart and peripheral circulation. Experiments were performed in 14 anesthetized dogs in order to determine whether programmed ventricular stimulation produces changes in renal sympathetic nerve activity; quantitate these changes; and determine the cardiovascular reflexes that mediate these changes. Arterial and right atrial pressures and renal sympathetic nerve activity were recorded in dogs before and after administration of single and double programmed ventricular stimuli. In a group of 10 dogs after single extrastimuli, diastolic arterial pressure decreased by 18 +/- 2 mm Hg (mean +/- SEM) while renal sympathetic nerve activity increased by 39 +/- 15 impulses/s. These changes were directly related to degree of stimulus prematurity. After double extrastimuli, diastolic arterial pressure decreased by 22 +/- 2 mm Hg whereas renal sympathetic activity increased by 55 +/- 8 impulses/s. In an additional four dogs, double extrastimuli decreased arterial pressure (-34 +/- 1 mm Hg) and increased cardiac (86 +/- 16%) and renal (82 +/- 12%) sympathetic traffic. After sinoaortic denervation, neither single nor double programmed ventricular stimuli resulted in alterations in cardiac or renal sympathetic nerve activity. It is concluded that the decreased arterial pressure caused by single and double programmed ventricular stimuli leads to increases in cardiac and renal sympathetic nerve activity that are mediated by sinoaortic baroreflexes.

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

Impairment of cardiopulmonary baroreflex after cardiac transplantation in humans.

There is ample evidence for efferent cardiac denervation in patients after cardiac transplantation. However, little is known regarding the effects of the cardiac deafferentation that also results. We examined responses to graded lower-body negative pressure and thus cardiopulmonary baroreceptor unloading in 23 patients 3 to 12 months after cardiac transplantation and compared their responses with those of nine normal subjects. Responses of mean arterial pressure, forearm vascular resistance, and plasma norepinephrine were assessed during lower-body negative pressure and the cold pressor test. Reflex increases in forearm vascular resistance (1.5 +/- 1, 5.0 +/- 1.4, and 6.4 +/- 2.1 vs 14.5 +/- 4.5, 20.3 +/- 6.5, and 34 +/- 11 units) and plasma norepinephrine (42 +/- 12, 58 +/- 15, and 62 +/- 13 vs 49 +/- 14, 94 +/- 25, and 173 +/- 36 pg/ml) during lower-body negative pressure (at -10, -20, and -40 mm Hg) were strikingly smaller in cardiac transplant patients than in normal subjects. The impaired responses of the cardiac transplant patients were not the result of a nonspecific depression of cardiovascular reflexes, since increases in mean arterial pressure (12 +/- 3 vs 10 +/- 2 mm Hg), forearm vascular resistance (19.5 +/- 3.4 vs 18 +/- 5.8 units), and plasma norepinephrine (56 +/- 8 vs 42 +/- 11 pg/ml) during cold pressor test were not significantly different in the two groups. Furthermore, the impaired responses were not caused by the immunosuppressive agents used to treat the cardiac transplant patients, since patients with renal transplants on similar regimens had augmented forearm vasoconstrictor responses.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1987

Effects of hydrochlorothiazide and diltiazem on reflex vasoconstriction in hypertension.

The purpose of our study was to determine the effects of treatment with hydrochlorothiazide (n = 10) or diltiazem (n = 8) on reflex humoral, hemodynamic, and vascular responses to graded lower body negative pressure in subjects with mild to moderate hypertension (supine diastolic pressure, 95-114 mm Hg). All subjects received placebo for 2 to 4 weeks followed by either hydrochlorothiazide (25-50 mg b.i.d.) or diltiazem (120-180 mg b.i.d.) to achieve a reduction in supine diastolic pressure of 10 mm Hg or more and a final pressure below 90 mm Hg. Mean arterial pressure, forearm vascular resistance, plasma norepinephrine, and renin responses to graded lower body negative pressure (-10, -20, -40 mm Hg) and head-up tilt were examined before and after 12 weeks of treatment with either drug. Pretreatment basal values of mean arterial pressure (114 +/- 2 vs 117 +/- 2 mm Hg), forearm vascular resistance (29 +/- 3 vs 35 +/- 7 units), and plasma renin activity (0.7 +/- 0.2 vs 0.6 +/- 0.2 ng angiotensin I/ml/hr) were not significantly different between groups. There were no significant differences in basal plasma norepinephrine or in the increases of norepinephrine in response to lower body negative pressure before and after treatment in either group. Forearm vascular resistance responses to lower body negative pressure were virtually abolished in the diltiazem-treated group but not in the hydrochlorothiazide-treated group despite similar levels of mean arterial pressure and basal forearm vascular resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1987

Impaired responses of sympathetic nerves to cardiac receptor stimulation in hypertension.

We recently reported that the vagal cardiopulmonary baroreceptor reflex inhibition of renal nerve traffic is impaired in rabbits with renal hypertension. The purpose of this study was to determine if the locus of the abnormality is mainly in the brain or in the afferent limb of the reflex. Experiments were done in alpha-chloralose-anesthetized rabbits with (n = 10) or without (n = 10) hypertension induced 6 to 8 weeks before study by wrapping the left kidney in cellophane followed by removal of the right kidney. The left side of the chest was opened, and a pericardial cradle was made. Nicotine was applied to the epicardial surface of the heart in concentrations of 10 to 500 micrograms/ml, and changes in arterial pressure and renal nerve traffic were measured. Dose-dependent decreases in traffic and arterial pressure resulted that were significantly smaller in hypertensive than in normotensive rabbits. After sinoaortic baroreceptor denervation, a similar impairment in the responses of hypertensive rabbits was observed. Vagotomy nearly abolished the responses of the renal nerves to epicardial nicotine. The responses of the lumbar sympathetic nerves to epicardial nicotine also were impaired in renal hypertensive (n = 8) compared with normotensive rabbits (n = 8). If the behavior and number of chemically sensitive endings are assumed to be unaltered in hypertension, then these findings are explained best by an abnormality in the central nervous system. These results support the view that the previously reported impairment in the vagal cardiopulmonary baroreceptor reflex control of renal nerve traffic is due mainly to a central abnormality, although they do not exclude an abnormality in the afferent limb of the reflex.

Animals↗

PubMed1987

Reflex vasoconstrictor responses to cardiopulmonary baroreceptor unloading, head-up tilt, and cold pressor testing in elderly mild-to-moderate hypertensives: effect of clonidine.

To determine whether clonidine treatment affects cardiopulmonary baroreflex induced sympathetic activation, we assessed the hemodynamic and hormonal responses to lower body negative pressure (LBNP) before and after 3 weeks of treatment with low-dose (0.2 mg daily) clonidine in eight older (mean age, 62 years) patients with established mild-to-moderate hypertension. Arterial pressure, heart rate (HR), forearm vascular resistance (FVR), plasma norepinephrine (NE), and renin activity (PRA) responses were assessed. Our results demonstrate that clonidine treatment had no effect on basal or stimulated PRA and plasma NE levels at baseline and during LBNP. Baseline FVR significantly decreased (48 +/- 3 to 35.5 +/- 6 U) and the FVR responses to LBNP were lower following clonidine therapy. Although baseline mean arterial pressure (MAP) and FVR as well as FVR responses to LBNP were lower after clonidine, the responses to tilt and cold pressor testing were unchanged. Thus clonidine appears to act via peripheral mechanisms, as well as by decreasing central sympathetic outflow to lower peripheral vascular resistance.

Aged↗

PubMed1987

Control of lumbar sympathetic nerve traffic by vagal cardiopulmonary baroreflexes in renal hypertension.

Renal nerve traffic is inhibited during volume expansion mainly because of stimulation of vagal cardiopulmonary baroreflexes. These responses are impaired in rabbits with renal hypertension caused by impaired cardiopulmonary baroreflexes. Previous studies have suggested that there may be differences in the extent to which renal hypertension alters reflex control of lumbar as compared with renal sympathetic nerve activity. The goals of this study were to determine if the responses to volume expansion of lumbar sympathetic nerve traffic also are impaired in renal hypertension and if this abnormality, if present, is caused by abnormalities in the vagal cardiopulmonary baroreflex. Experiments were done in alpha-chloralose-anesthetized normotensive (n = 9) and renal hypertensive (n = 7; 1 kidney, 1 wrap) rabbits. Infusion of dextran in saline raised arterial and left atrial pressures in both groups and decreased lumbar nerve traffic by -4.4 +/- 0.4% mm Hg rise in arterial pressure in the normotensive group and by -1.5 +/- 0.1% mm Hg in the hypertensive group (p less than 0.01). These responses were nearly abolished by sinoaortic denervation in both groups. These data indicate that the responses of lumbar nerve traffic to volume expansion are impaired in renal hypertension; this is mainly because of impaired arterial baroreflexes since vagal cardiopulmonary baroreceptors have minimal influence on lumbar nerve traffic, even in normotensive rabbits. These findings for the lumbar nerves are strikingly different from those reported previously for reflex control of the renal nerves in both normotensive and hypertensive rabbits.

Animals↗

PubMed1986

Afferent reinnervation of the autotransplanted heart in dogs.

Patients have been observed with a chest pain syndrome after cardiac transplantation. For this pain to be cardiac in origin the afferent nerves carrying sensory information from the heart would have to reinnervate the heart. A previous study in dogs indicated that afferent reinnervation is uncommon during the first 2 years after transplantation. The purpose of this study was to determine whether afferent reinnervation of the heart occurs in the long term. The decreases in arterial pressure and renal nerve activity resulting from chemical stimulation of left ventricular sensory receptors with vagal afferents with cryptenamine (veratrum alkaloid) were assessed in three dogs 8 to 12 years and in four dogs 6 to 8 weeks after cardiac autotransplantation and in six sham-operated dogs (thoracotomy-pericardiotomy 6 to 8 weeks before study). Responses of renal nerve activity to physiologic stimulation of cardiac receptors by volume expansion were also determined. Left ventricular cryptenamine inhibited renal nerve activity by 72 +/- 8% in dogs with long-term and by 10 +/- 6% in dogs with short-term autotransplantation and by 92 +/- 5% in sham-operated dogs. Decreases in mean arterial pressure in these groups were 34 +/- 4, 11 +/- 3 and 67 +/- 16 mm Hg, respectively. Volume expansion inhibited renal nerve activity in long-term autotransplant (43%) and sham-operated (48%) groups but less in the short-term transplant group (33%) for comparable increases in cardiac filling pressure. It is concluded that in dogs there is extensive afferent reinnervation of the long-term autotransplanted heart that results in relatively normal cardiopulmonary baroreflex responses to volume expansion.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗

PubMed1986

Myocardial norepinephrine, epinephrine and dopamine concentrations after cardiac autotransplantation in dogs.

Myocardial norepinephrine is markedly reduced after cardiac transplantation because of interruption of postganglionic cardiac sympathetic nerves. There are also substantial stores of dopamine in the myocardium, but the influence of cardiac denervation on dopamine remains unknown. The effect of cardiac transplantation was determined and, thus, the effect of denervation on myocardial norepinephrine, dopamine and epinephrine. Myocardial catecholamines were measured with high-performance liquid chromatography with electrochemical detection in five dogs 6 to 8 weeks and in four dogs 8 to 12 years after cardiac autotransplantation and in six sham-operated dogs with intact cardiac innervation. Norepinephrine, dopamine and epinephrine levels were determined from samples obtained from the right and left atria and ventricles. Samples from the left ventricular apex and base were analyzed separately. There was a striking depletion of norepinephrine in all cardiac chambers after short-term autotransplantation. The norepinephrine content of the left atrium in sham-operated dogs (1,659 +/- 219 ng/g) was significantly higher than that of dogs with long-term autotransplanted hearts (754 +/- 372 ng/g). Sham-operated dogs and dogs with long-term autotransplanted hearts had statistically significant (p less than 0.05) differences in norepinephrine content in the left ventricular apex (480 +/- 197 versus 294 +/- 198 ng/g), left ventricular base (876 +/- 2204 versus 654 +/- 156 ng/g) and right ventricle (766 +/- 133 versus 247 +/- 29 ng/g). In contrast to norepinephrine, dopamine concentrations were relatively preserved in the short-term group despite the virtual depletion of myocardial norepinephrine.(ABSTRACT TRUNCATED AT 250 WORDS)

Aluminum Oxide↗

PubMed1986

Influence of intravenous and intracerebroventricular vasopressin on baroreflex control of renal nerve traffic.

We performed experiments in alpha-chloralose-anesthetized rabbits with vagi sectioned, to determine the influence of intravenous and intracerebroventricular vasopressin on arterial baroreflex control of renal nerve activity. Arterial baroreflex control of renal nerve activity was assessed during phenylephrine-induced increases and nitroglycerin-induced decreases in arterial pressure. Intravenous vasopressin (4 and 40 mU over 1 minute) reduced basal renal nerve activity (from 149 +/- 14 to 101 +/- 13 and 28 +/- 13 impulses/sec) without changing arterial pressure and reduced the sensitivity of the arterial baroreflex control of renal nerve activity. This effect was reversed by vasopressin antagonist (d(CH2)5[Tyr(Me)2]AVP) which blocks vasoconstrictor effects of vasopressin. Intracerebroventricular vasopressin (4, 40, or 400 mU) did not alter basal renal nerve activity or arterial pressure but increased the sensitivity of baroreflex control of renal nerve activity. This effect was not blocked by the vasopressin antagonist. The influence of intravenous vasopressin on basal renal nerve activity was not altered by sinoaortic baroreceptor denervation. In contrast, the inhibitory influence of intravenous vasopressin on lumbar sympathetic nerve activity was abolished by sinoaortic denervation. Finally, intravenous vasopressin inhibited renal nerve activity (by 43 +/- 5%) in six rabbits with spinal cord transection. This effect was abolished by the vasopressin antagonist. We draw the following conclusions from these data: (1) intravenous and intracerebroventricular vasopressin have different effects on basal and baroreflex control of renal nerve activity; (2) these effects are mediated by different vasopressin receptors; (3) the effects of intravenous vasopressin on basal renal nerve activity are not baroreflex dependent, and appear to be mediated by spinal or, possibly, ganglionic mechanisms.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1985

Effects of diltiazem on hormonal and hemodynamic responses to lower body negative pressure and tilt in patients with mild to moderate systemic hypertension.

Mean arterial blood pressure, forearm vascular resistance, plasma norepinephrine, plasma renin activity and aldosterone responses to graded lower body negative pressure and tilt at 80 degrees were examined in 10 men with mild to moderate essential hypertension before and after 12 weeks of diltiazem (240 to 360 mg/day) therapy. Diltiazem therapy lowered basal supine systolic and diastolic blood pressures without affecting basal heart rate. Mean arterial blood pressure and forearm vascular resistance were decreased from 114 +/- 1.5 to 105 +/- 1 mm Hg, p less than 0.01 and from 29.3 +/- 3.5 to 18.9 +/- 2.1 units, p less than 0.01, respectively. Diltiazem therapy had no effect on basal supine levels of norepinephrine, plasma renin activity or aldosterone, nor on the responses of these hormones to lower body negative pressure. Diltiazem did decrease the forearm vascular resistance responses to lower body negative pressure and tilt. Diltiazem abolished an orthostatic increase (10 +/- 0.3 mm Hg) in mean arterial blood pressure and this was associated with a greater plasma norepinephrine response to tilt. These results suggest that diltiazem decreases vascular resistance through a reduction in the postjunctional effects of norepinephrine on vascular smooth muscle.

Adult↗