Biomedical subjects

C M Heesch

Publications and source records attributed to C M Heesch.

At least 37 records · Page 2Linked to original sources

PubMed1994

Effect of metoprolol on myocardial function and energetics in patients with nonischemic dilated cardiomyopathy: a randomized, double-blind, placebo-controlled study.

OBJECTIVES: This study examined the effects of metoprolol on left ventricular performance, efficiency, neurohormonal activation and myocardial respiratory quotient in patients with dilated cardiomyopathy. BACKGROUND: The mechanism by which beta-adrenergic blockade improves ejection fraction in patients with dilated cardiomyopathy remains an enigma. Thus, we undertook an extensive hemodynamic evaluation of this mechanism. In addition, because animal models have shown that catecholamine exposure may increase relative fatty acid utilization, we hypothesized that antagonism of sympathetic stimulation may result in increased carbohydrate utilization. METHODS: This was a randomized, double-blind, prospective trial in which 24 men with nonischemic dilated cardiomyopathy underwent cardiac catheterization before and after 3 months of therapy with metoprolol (n = 15) or placebo (n = 9) in addition to standard therapy. Pressure-volume relations were examined using a micromanometer catheter and digital ventriculography. RESULTS: At baseline, the placebo-treated patients had somewhat more advanced left ventricular dysfunction. Ejection fraction and left ventricular performance improved only in the metoprolol-treated patients. Stroke and minute work increased without an increase in myocardial oxygen consumption, suggesting increased myocardial efficiency. Further increases in ejection fraction were seen between 3 and 6 months in the metoprolol group. The placebo group had a significant increase in ejection fraction only after crossover to metoprolol. A significant relation between the change in coronary sinus norepinephrine and myocardial respiratory quotient was seen, suggesting a possible effect of adrenergic deactivation on substrate utilization. CONCLUSIONS: These data demonstrate that in patients with cardiomyopathy, metoprolol treatment improves myocardial performance and energetics, and favorably alters substrate utilization. Beta-adrenergic blocking agents, such as metoprolol, are hemodynamically and energetically beneficial in the treatment of myocardial failure.

Cardiac Catheterization↗

PubMed1994

Magnesium in acute myocardial infarction.

Clinical studies on the use of magnesium in acute myocardial infarction have yielded contradictory results. While the exact reasons for these discrepancies are unclear, it appears that the timing of magnesium administration is crucial to the success or failure of therapy. Although some studies have shown a significant reduction in the odds of death with this agent, the exact reasons underlying this possible benefit are not yet fully understood. A reduction in arrhythmias, inhibition of thrombus generation, changes in coronary and peripheral hemodynamics, and the limitation of ischemic damage and reperfusion injury have been inferred as possible mechanisms. IV magnesium is inexpensive and easy to administer, and has minimal side effects. While further research on magnesium therapy in ischemic states is warranted, the early use of IV magnesium should be considered in selected patients with suspected acute myocardial infarction.

Drug Administration Schedule↗

PubMed1993

Pregnancy restores the renal vasodilator response to glycine in Dahl salt-sensitive rats.

To determine if pregnancy alters the impaired renal vasodilator responses in hypertensive Dahl salt-sensitive (Dahl S) rats, we measured glomerular filtration rate and effective renal plasma flow and calculated renal vascular resistance before, during, and after renal vasodilation with glycine (0.17 mmol/kg per minute IV). Conscious, midterm (day 11 to 14) pregnant and age-matched virgin Dahl S and Dahl salt-resistant (Dahl R) rats were fed an 8% NaCl diet for 4 weeks (n = 6 per group). Mean arterial pressure was elevated (P < .05) in Dahl S compared with Dahl R rats, with no significant difference between pregnant and virgin animals in either group. Pregnancy resulted in significant increases in plasma volume, baseline glomerular filtration rate, and renal plasma flow and a significant decrease in renal vascular resistance. The glycine-induced increase in filtration rate in virgin Dahl S rats (27 +/- 4%) was less (P < or = .01) than pregnant Dahl S (60 +/- 4%) and either group of Dahl R (virgin, 43 +/- 3%; pregnant, 45 +/- 5%) rats. Similarly, the 21 +/- 4% increase in renal plasma flow in virgin Dahl S rats was less (P < or = .01) than the pregnant Dahl S (45 +/- 4%) and either pregnant (45 +/- 5%) or virgin (45 +/- 5%) Dahl R rats. Glycine decreased renal vascular resistance only 12 +/- 2% in the virgin Dahl S compared with 31 +/- 3% in the pregnant Dahl S rats and 30 +/- 4% and 28 +/- 3% in pregnant and virgin Dahl R rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗

PubMed1992

Is there a central nervous system component to acute baroreflex resetting in rats?

This study was designed to evaluate a possible central nervous system (CNS) component to acute baroreflex resetting. In nine arterial baroreceptor-denervated, chloralose-urethan-anesthetized rats, a control (C) aortic nerve stimulation curve (3-5 V, 1 ms, 0-64 Hz) was obtained. Next, a constant "baroreceptor" input was delivered to the CNS (left aortic nerve stimulation, 10 min, 10.2 +/- 1.5 Hz). Within the first 13 s of aortic nerve stimulation, maximum inhibition of lumbar sympathetic nerve activity (LSNA) was 60 +/- 7.8% of baseline and at 1 min it increased to 68 +/- 5.6% of baseline. At the end of the 10-min aortic nerve stimulation, LSNA was not different from the response at 1 min (68 +/- 5.6% = 74 +/- 4.1%). Immediately after the constant stimulation (within 30 s), a test or reset (RS) curve was obtained (0-64 Hz). A recovery (RC) curve was obtained 10-20 min later. The slope of the linear portion of the curve and the stimulation frequency that produced 50% maximum inhibition (ES50) were compared among the three baroreflex curves (C, RS, RC,) and no significant differences were found. Thus, although a CNS component to baroreflex adaptation was evident during the first minute of aortic nerve stimulation, a longer term acute resetting of the baroreflex curve did not occur.

Animals↗

PubMed1990

Cardiovascular effects of posterior hypothalamic stimulation in baroreflex-denervated rats.

The overall purpose of this study was to examine the effect of sinoaortic baroreceptor denervation (SAD) on the cardiovascular and sympathetic outflow responses to electrical stimulation of the posterior hypothalamus. In anesthetized rats that had undergone SAD 7-10 days before experimentation, electrical stimulation of the posterior hypothalamus elicited greater increases in mean arterial pressure, iliac vascular resistance, mesenteric vascular resistance, and lumbar sympathetic nerve activity than in sham-operated baroreceptor-intact animals. Similarly, the pressor effects of intravenous norepinephrine were also augmented in the baroreceptor-denervated group compared with the baroreceptor-intact group. When posterior hypothalamic and intravenous norepinephrine pressor stimuli, which produced equivalent pressor responses in sham-operated baroreceptor-intact animals, were compared in baroreceptor-denervated animals, the pressor effects of the central hypothalamic stimulus were enhanced to a greater degree than the norepinephrine pressor effects. These data provide evidence that arterial baroreceptor reflexes exert greater buffering of pressor stimuli initiated from the central nervous system compared with pressor responses due to peripheral vascular vasoconstrictor agents.

Animals↗

PubMed1990

Nicotine-induced skeletal muscle vasodilation is mediated by release of epinephrine from nerve terminals.

To determine the role of sympathetic innervation on nicotine-induced alterations in peripheral (hindlimb) blood flow in the pentobarbital-anesthetized dog, one hindlimb was acutely denervated and remained attached to the body by only the femoral artery and vein, whereas the contralateral limb remained innervated and intact. Measurements were made of aortic pressure, femoral artery and venous pressures, femoral artery flow, and plasma catecholamine levels during intravenous systemic infusion of nicotine. The response to nicotine (9-36 micrograms.kg-1.min-1) on the denervated side was a transient increase followed by a persistent decrease in flow and increase in vascular resistance. The response in the innervated limb was a large increase in blood flow and decrease in vascular resistance. The vasoconstrictor and vasodilator responses could be abolished by pretreatment with both propranolol and phentolamine. The vasodilator response could not be abolished by cholinergic or histaminergic receptor antagonism. Hexamethonium abolished all systemic and peripheral responses to nicotine. Desipramine selectively abolished the vasodilator response in the innervated hindlimb. The vasodilator and vasoconstrictor responses could be mimicked with systemic or local administration of epinephrine. We conclude that, in the hindlimbs of dogs, nicotine stimulates the release of epinephrine from nerve terminals and/or tissue stores to activate beta 2-adrenoceptors and promote vasodilation in skeletal muscle of innervated preparations.

Adrenalectomy↗

PubMed1990

Baroreflex control of sympathetic outflow in pregnant rats: effects of captopril.

Arterial baroreflex control of renal sympathetic nerve activity (RSNA) was compared in nonpregnant (NP) and near-term pregnant (P) chloralose-anesthetized rats. Baroreflex curves were obtained by recording reflex changes in RSNA (expressed as a percent of base line) due to increases and decreases in mean arterial pressure (MAP) [intravenous phenylephrine and nitroprusside (NTP)]. The slope, midpoint (EP50), and threshold pressures of the baroreflex curves were compared. Base-line MAP was significantly lower in the pregnant animals (P = 96 +/- 3 vs. NP = 113 +/- 5 mmHg). The baroreflex curves of pregnant animals also had significantly lower threshold (P = 95 +/- 3 vs. NP = 110 +/- 5 mmHg) and midpoint values (P = 105 +/- 4 vs. NP = 119 +/- 5 mmHg). The response to unloading the baroreceptors was attenuated in the pregnant animals as indicated by a decrease in slope of the NTP portion of the baroreflex curve (P = 0.95 +/- 0.17 vs. NP = 1.61 +/- 0.29% nerve activity/mmHg). Responses to blockade of angiotensin-converting enzyme with captopril (2 mg/kg iv) were also examined. There were no differences in EP50 or slope among the control, captopril, and recovery baroreflex curves within either the nonpregnant or pregnant animals. However, after captopril, MAP decreased to a greater extent in the pregnant rats, yet RSNA increased to the same level for the two groups. Thus pregnancy results in a leftward shift of the baroreflex function curve toward a lower operating pressure range. In addition, pregnant rats demonstrated an impaired ability to increase sympathetic outflow above base-line values in response to a hypotensive challenge.

Animals↗

PubMed1989

Response of the arteriolar network in rat cremaster muscle to intraarterial infusion of nicotine.

The response of the arteriolar network in rat cremaster muscle to continuous intraarterial infusion of nicotine was studied. Measurements were made of mean femoral arterial pressure, inside vessel diameter, red blood cell velocity and volumetric flow rate in each of four series-coupled arteriolar segments. Nicotine was continuously infused in a cumulative fashion in doses of 12.5, 25, 50 and 100 micrograms/kg/min. After a 10 min infusion of each dose, measurements were made again in each arteriole and compared with the values obtained prior to infusion of nicotine. Arterial pressure increased in a graded fashion with increasing dose of nicotine up to 50 micrograms/kg/min. The smaller arterioles demonstrated a dose dependent vasoconstriction and reduction in flow rate which were maximal at a dose of 50 micrograms/kg/min. In another series of experiments, the microvascular responses to nicotine infusion were obtained in the acutely denervated microvasculatured. The nicotine-induced flow reduction was significantly diminished by denervation. In a separate series of experiments nicotine was infused at doses of 25 and 50 micrograms/kg/min, and plasma catecholamine concentrations were determined. Plasma norepinephrine and epinephrine were significantly elevated at only the higher dose. Responses in denervated tissues suggest that plasma catecholamine concentrations were approximately threshold for arteriolar responses. It is concluded that the nicotine-induced flow reduction in rat skeletal muscle is due primarily to enhanced release of norepinephrine from vasomotor nerves with little or no influence from circulating catecholamines.

Animals↗

PubMed1988

Effects of chronic smoke exposure on the cardiovascular responses to acute nicotine infusion in the rat.

Rats were exposed daily to cigarette smoke for 17-22 weeks in order to characterize mean arterial pressure and regional hemodynamic effects of chronic smoke exposure and to determine if cardiovascular reactivity to acute nicotine infusions is altered by chronic smoke exposure. Urethane-anesthetized animals were instrumented with miniaturized pulsed-Doppler flow probes on the iliac and mesenteric vascular beds. Under resting conditions sham-smoked and smoke-exposed animals had similar levels of mean arterial pressure and mesenteric blood flow; however, resting heart rate was lower in the smoke-exposed group, while iliac blood flow was elevated in the smoke-exposed group. Acute nicotine infusion (6.25, 12.5 and 25 micrograms/kg per min) produced equivalent, dose-dependent pressor effects as well as increases in iliac and mesenteric resistance in sham and smoke-exposed groups. Thus, chronic cigarette smoke-exposure in rats may exert significant cardiovascular effects other than on arterial pressure such as lowered heart rate and elevated blood flow to skeletal muscle beds, while cardiovascular responses to nicotine are not altered by chronic smoke-exposure.

Animals↗

PubMed1987

Acute resetting of arterial baroreflexes in hypertensive rats.

Acute baroreflex resetting was studied in one-kidney, one-clip renal hypertensive (HT) and normotensive (NT) control male Wistar-Kyoto rats. Systolic blood pressure (SBP) was monitored weekly in conscious rats by the indirect tail-cuff occlusion method. At the time of experimentation (4-6 wk after placement of the clip), SBP in the HT rats (238 +/- 9 mmHg) was elevated compared with NT rats (117 +/- 5 mmHg). Baroreflex control of lumbar sympathetic nerve activity (LSNA) was assessed in alpha-chloralose (120 mg/kg)-urethan (600 mg/kg)-anesthetized rats by raising and lowering mean arterial pressure (MAP) between 50 and 200 mmHg (phenylephrine and nitroprusside infusions). The baroreflexes of the hypertensive rats were less sensitive to increments in pressure compared with normotensive rats as evidenced by a decreased slope of the baroreflex curve (-0.396 +/- 0.064 HT vs. -0.637 +/- 0.042 NT). In both groups, curves were obtained before (control) and after (reset) base-line MAP was increased by 30-55 mmHg for 15 min. The MAP for 50% maximum inhibition of LSNA (EP50) was increased in both groups of rats after exposure to the elevated pressure (NT, control = 109 +/- 5.2, reset = 120 +/- 5.0 mmHg; HT, control = 114 +/- 6.5, reset = 131 +/- 10.0 mmHg) with no significant change in slope. There was no significant difference in degree of upward resetting between the two groups (NT, 21 +/- 4%; HT, 30 +/- 7%). Thus, although hypertensive rats exhibited the depressed baroreflex function associated with chronic resetting, the ability to reset acutely was maintained.

Animals↗

PubMed1987

Interactions in nucleus tractus solitarius between right and left carotid sinus nerves.

Bilateral carotid sinus nerve stimulation was used as a model for studying cardiovascular afferent interactions in the nucleus tractus solitarius (NTS) region of dorso-medial medulla. Extracellular action potential recordings were made from 69 single units, 33 of which were excited independently by both right and left carotid sinus nerves (CSNs). Fifteen of these were located in NTS. Peak latencies to electrical stimulation of NTS neurons were 17.7 +/- 2.1 ms to ipsilateral CSN and 20.9 +/- 1.5 ms to contralateral CSN. Summation of afferent input was routinely demonstrated. In 10 units in NTS, a conditioning stimulus applied to one CSN caused prolonged inhibition of the response to a test stimulus to the same or the other CSN. The duration of inhibition was dependent on the intensity of the conditioning stimulus, not on prior excitation of the unit by the conditioning stimulus. In five additional excitability testing experiments, we found limited evidence to suggest that primary afferent depolarization of the central fibers of one CSN by stimulation of the contralateral CSN might be contributing to this inhibitory interaction. The data suggest that the outcome of integrative interactions between right and left CSN inputs to NTS neurons may depend largely on the temporal sequence of convergent afferent impulses.

Action Potentials↗

PubMed1987

Prevention or attenuation of baroreceptor resetting by pulsatility during elevated pressure.

Acute static elevation of arterial pressure increases the pressure threshold for activation of baroreceptors (acute resetting). The purpose of this study was to test the hypothesis that pulsatility during acute elevation of pressure modifies this acute resetting. Activity was recorded in 21 single baroreceptor units from the isolated carotid sinuses of dogs anesthetized with chloralose. Single-unit pressure thresholds were determined with a slow ramp increase in pressure. After a control period of static pressure at 25 to 50 mm Hg, the pressure threshold averaged 69 +/- 4 (SE) mm Hg. Three graded levels of static pressure were held for 5 to 15 minutes. The levels averaged 76 +/- 4, 115 +/- 6, and 170 +/- 5 mm Hg. The corresponding nerve activity during these periods was 0, 44 +/- 6, and 63 +/- 6 spikes per second, and the resulting increases in pressure threshold averaged 10 +/- 1, 17 +/- 2, and 26 +/- 3 mm Hg, respectively. In contrast, during equivalent elevations of pulsatile pressure, nerve activity averaged 20 +/- 3, 37 +/- 4, and 61 +/- 5 spikes per second, and the increases in pressure threshold averaged 0 +/- 4, 14 +/- 2, and 24 +/- 2 mm Hg, respectively. In some units, the pressure threshold decreased following elevation of pulsatile pressure. The results indicate that: pulsatility during elevation in pressure prevents or attenuates the acute baroreceptor resetting except at maximal pressure; upward resetting occurs with elevation of static pressure even when there is no nerve activity during the period of elevated pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1987

Neural modulation of transcapillary exchange of fluid and solutes in whole-organ preparations.

Activation of sympathetic adrenergic postganglionic fibers that release norepinephrine at the neuromuscular junction can influence resistance, capacitance, and exchange functions in the microcirculation. Although the predominant response is an increase in precapillary resistance that reduces blood flow through the tissue (at constant pressure perfusion), there are two distinct components that can be separated into an initial (1-2-minute) and late (2-15-minute) response. The initial (1-2-minute) response is a decrease in venous and capillary pressures in passive response to decreased flow promoted by an increase in precapillary resistance. Venous pressures are reduced even though postcapillary resistance is increased. The decrease in capillary pressure promotes absorption of fluid from tissue to plasma. Venous constriction results in a translocation of blood from the terminal venous system into the larger venous conduits toward the heart. Total blood volume in an isolated organ system decreases and is manifested as a decrease in volume (plethysmographic) or weight (gravimetric). The decrease in volume is result of three interrelated factors: 1) decrease in flow through the organ, 2) active venoconstriction and a translocation of blood out of the organ, and 3) absorption of fluid from tissue to plasma, which flows out of the organ with venous drainage. With continued sympathetic nervous system stimulation, the late response (3-15 minutes) is a gradual decrease in precapillary resistance that increases blood flow through the organ. Venous and capillary pressures passively increase in association with increases in flow.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1984

Acute resetting of carotid sinus baroreceptors. I. Dissociation between discharge and wall changes.

The purpose of this study was to assess whether mechanical changes in the carotid sinus wall could account for acute resetting of the carotid sinus baroreceptors in chloralose-anesthetized dogs. Threshold pressure and pressure-discharge curves for single-unit baroreceptors were determined before and after the vascularly isolated carotid sinus was exposed to brief increases or decreases in base-line pressure. When intrasinus pressure was increased by 30 mmHg for 15 min, threshold pressure increased by 9 +/- 1.3 (SE) mmHg (n = 12), and when intrasinus pressure was decreased by 30 mmHg threshold pressure decreased by 14 +/- 4.2 mmHg (n = 9), with no change in gain of the pressure-discharge curves. In 14 experiments carotid sinus pressure was increased from 70 (control) to 160 mmHg for only 5 min (reset) and returned to 70 mmHg for 10 min (recovery). After exposure to the higher pressure, threshold pressure increased from 75 +/- 3.8 to 94 +/- 4.4 mmHg, and carotid sinus diameter (sonomicrometer) and calculated wall strain at each pressure increased. After the recovery period, baroreceptor threshold pressure returned to 75 +/- 4.1 mmHg, but diameter and wall strain remained elevated. We interpret our finding that baroreceptor resetting and recovery are not accompanied by reciprocal changes in carotid sinus diameter to indicate that a mechanical mechanism alone cannot explain acute resetting.

Animals↗

PubMed1984

Acute resetting of carotid sinus baroreceptors. II. Possible involvement of electrogenic Na+ pump.

In the accompanying manuscript [Am. J. Physiol. 247 (Heart Circ. Physiol. 16): H824-H832, 1984] we demonstrated that a mechanical mechanism alone cannot account for acute resetting of baroreceptors. To determine if changes in the activity of a baroreceptor electrogenic Na+ pump contributed to resetting, single-unit baroreceptor discharge was recorded from the carotid sinus nerve while resetting protocols were performed before and after exposing the vascularly isolated carotid sinus to treatments known to block the Na+ pump [ouabain and low extracellular K+ concentration ([K+]o)]. Ouabain (0.1-0.5 microgram/ml) blocked the increase in baroreceptor threshold pressure that occurred when intrasinus pressure was increased by 30 mmHg for 15 min [delta threshold = 16 +/- 3 (SE) mmHg before and 1.2 +/- 2.3 mmHg after ouabain]. In 12 experiments carotid sinus pressure was increased from 70 to 160 mmHg for 5 min and then returned to 70 mmHg for 10 min in the presence of both normal [K+]o (5.8 mM) and low [K+]o. Exposure to the low K+ solution resulted in a significantly smaller increase in threshold pressure when intrasinus pressure was increased from 70 to 160 mmHg (9 +/- 2.7 vs. 18 +/- 2.1 mmHg). When K+ was replaced, threshold pressure again increased by 18 +/- 2.3 mmHg, the increase in threshold was reversed. Thus, since ouabain blocked and low [K+]o attenuated acute resetting of the baroreceptors, we propose that changes in the activity of an electrogenic Na+ pump contribute to acute resetting.

Animals↗

PubMed1983

Reflex modulation of carotid sinus baroreceptor activity in the dog.

Carotid sinus baroreceptor (CBR) sensitivity may be increased by electrical stimulation of sympathetic nerves passing to the carotid sinus region. It remains unknown if reflexly induced changes in efferent sympathetic discharge affect CBR function. In 17 anesthetized dogs, we reflexly induced alterations in sympathetic discharge and recorded CBR activity originating from a vascularly isolated carotid sinus. The stimulus to the baroreceptors was pulsatile with constant mean and pulse pressure. Occlusion of the contralateral common carotid artery (n = 6) resulted in a reflex increase in arterial pressure (116 +/- 10 to 153 +/- 14 mmHg) and an increase (121 +/- 2% of control) in baroreceptor activity (P less than 0.05). Inferior vena caval occlusion (n = 6), which induced a reduction in arterial pressure (145 +/- 19 to 75 +/- 21 mmHg), also provoked an increase (141 +/- 10% of control) in baroreceptor discharge (P less than 0.05). Raising pressure (to 200 mmHg) in the contralateral carotid sinus (n = 7) resulted in a reflex decrease in arterial pressure (169 +/- 16 to 129 +/- 13 mmHg) and a reduction (82 +/- 3% of control) in baroreceptor activity (P less than 0.05). The changes in baroreceptor discharge were abolished by ipsilateral cervical sympathectomy or ganglionic blockade (n = 4). Our findings demonstrate that reflexly induced alterations in the activity of sympathetic fibers innervating the carotid sinuses can modulate baroreceptor discharge.

Animals↗

PubMed1983

Effects of calcium channel blockers on isolated carotid baroreceptors and baroreflex.

Our study determined the effects of the calcium antagonists, nifedipine and verapamil, on the carotid sinus baroreceptors and baroreflex. The left carotid sinus region in dogs was vascularly isolated and filled with oxygenated physiological salt solution. Steady-state multiunit activity was recorded from the carotid sinus nerve for sinus pressures of 50-200 mmHg after bathing the carotid sinus region in a solution containing no drug, 10 micrograms/ml nifedipine (n = 6), or 5 micrograms/ml verapamil (n = 5). The slopes of the curves relating carotid sinus nerve activity (% of maximum control) to carotid sinus pressure were control, 0.81 +/- 0.06; nifedipine, 1.29 +/- 0.14; and verapamil, 0.48 +/- 0.06%/mmHg, indicating that nifedipine increased and verapamil decreased the sensitivity of the carotid sinus baroreceptors. Additional studies with bilateral carotid sinus isolation (carotid sinus nerves intact) indicated that nifedipine enhanced and verapamil attenuated carotid baroreflex control of renal sympathetic nerve activity. Pressure-volume curves generated in the isolated carotid sinus showed that effects on smooth muscle do not account for the opposing effects of the two Ca2+ antagonists. Omitting Ca2+ from the physiological solution resulted in increased carotid sinus nerve activity, an effect blocked by verapamil but not nifedipine. Verapamil, but not nifedipine, inhibited veratrine-induced (Na+-dependent) excitation of carotid baroreceptors. Thus the excitatory effects of nifedipine on the carotid sinus baroreceptors are dependent on Ca2+ mechanisms, whereas the inhibitory effects of verapamil may be due mainly to interference with the inward Na+ current.

Animals↗

PubMed1982

Cardiovascular reflex modulation of plasma catecholamine concentrations in the anesthetized cat.

The purpose of this study was to examine the role of carotid sinus and cardiopulmonary mechanoreceptors in the reflex control of adrenal medullary catecholamine secretion. Afferent input from carotid sinus and cardiopulmonary mechanoreceptors was decreased by carotid occlusion or cervical vagal cold block, respectively. Increases in arterial pressure were significantly greater when either intervention was tested in the presence of the other, with the role of the carotid sinus baroreflex being dominant. Neither carotid occlusion nor vagal cold block resulted in a significant increase in plasma epinephrine or norepinephrine concentrations. However, carotid occlusion during vagal block caused a significant increase in plasma epinephrine (+87%) and norepinephrine concentrations (+128%). Likewise, vagal block during carotid occlusion increased plasma epinephrine (+82%) and norepinephrine concentrations (+73%). Similar experiments performed in a group of chemically sympathectomized animals (pre-treated with 50 mg/kg 6-hydroxydopamine) indicted that adrenal medullary norepinephrine as well as epinephrine release could be modulated by the carotid sinus and cardiopulmonary reflexes. Mean arterial blood pressure and heart rate were significantly lower in 6-hydroxydopamine-treated animals, compared with untreated controls. Although of lesser magnitude, responses to carotid occlusion and vagal block in 6-hydroxydopamine-treated animals were qualitatively similar to those in untreated animals. Plasma catecholamine concentrations did not increase from either manipulation. However, when the second manipulation was added to the first, significant increases occurred. We conclude from these data that both the carotid sinus and cardiopulmonary reflexes modulate the release of adrenal catecholamines. An interaction between the two reflexes exists whereby the influence of one reflex on catecholamine secretion is apparent only in the absence of the other input.

Animals↗