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PubMed1983

Suppressed basal antidiuretic hormone release during cyclooxygenase inhibition in conscious dogs.

Both in vitro and in vivo experiments suggest that prostaglandins may affect antidiuretic hormone (ADH) release centrally. In addition, other studies show that prostaglandins administered peripherally may cause ADH release. However, these latter studies have been flawed by hemodynamic alterations and the use of anesthetics, which make interpretation difficult. The present study was designed to test for involvement of prostaglandins produced outside the central nervous system in ADH release in conscious dogs. Administration of meclofenamate (2 mg/kg and 2 mg X kg-1 X h 1, iv) resulted in a consistent fall in plasma ADH levels in five dogs. This diminution of ADH release occurred with no change in systemic hemodynamics, arterial blood gases, or plasma osmolality, suggesting that prostaglandins are important mediators of basal ADH release in the conscious dog. Because meclofenamate does not cross the blood-brain barrier, prostaglandins produced outside the central nervous system appear to be involved in this process. The specific prostaglandin involved or the site of action of prostaglandins on ADH release is not clear at this time.

Animals↗
PubMed1984

Renal and iliac vascular responses to left ventricular receptor stimulation in conscious dogs.

The purpose of the present study was to investigate the relative responses of the renal and iliac vascular beds to the selective chemical stimulation of left ventricular receptors in the conscious dog. Twenty dogs were chronically instrumented to obtain measurements of arterial blood pressure, renal blood flow, and iliac blood flow before and after a bolus intracoronary injection of veratridine (0.4-1.0 micrograms/kg in 0.5-ml vol) with the heart paced. The responses to intracoronary veratridine were a significant reduction in arterial blood pressure averaging 25 mmHg accompanied by a simultaneous reduction in renal blood flow of 25%. Renal resistance did not change throughout the course of the response analyzed (50 s). Iliac blood flow, however, increased, reaching a peak of 35% above control due to a 51% decrease in iliac resistance. After sinoaortic denervation, renal resistance still failed to show a decrease, although the recovery of arterial blood pressure and iliac resistance was prolonged. After a mild hypotensive hemorrhage (20 ml/kg), a greater decrease in iliac resistance occurred with intracoronary veratridine injections, but renal resistance still did not change. The reduction in iliac resistance with intracoronary veratridine was significantly attenuated after phentolamine administration (2 mg/kg iv) but not after atropine alone (0.2 mg/kg iv). A significant cholinergic receptor component of iliac vasodilation was observed only after prior alpha-adrenergic-receptor blockade. The results of this study are consistent with the conclusion that in the conscious dog, left ventricular receptors exert a preferential neural control over skeletal muscle vascular resistance and do not influence renal vascular resistance.

Animals↗
PubMed1984

Activation of afferent renal nerves by intrarenal bradykinin in conscious rats.

Bradykinin was infused intravenously and into the right renal artery of conscious rats that were chronically instrumented with catheters and miniaturized pulsed-Doppler flow probes. The effects on regional hemodynamics were compared with those in animals in which the infused kidney was denervated as well as in animals anesthetized with pentobarbital sodium. In intact rats bradykinin (1 microgram/min) caused an immediate increase in mean arterial blood pressure (MAP, 27 +/- 4 mmHg), heart rate (HR, 67 +/- 11 beats/min), mesenteric resistance (MR, 32 +/- 10%), and both right (RRR, 42 +/- 14%) and left renal resistance (LRR 21 +/- 8%). These effects were significantly different from those during intravenous infusion of the same dose of bradykinin (MAP, 6 +/- 3 mmHg; HR, 31 +/- 7 beats/min; MR, -21 +/- 5%; RRR, 8 +/- 4%; LRR, 6 +/- 3%). Pentobarbital greatly attenuated the responses to intrarenal bradykinin. In conscious animals denervation of the infused kidney completely abolished the cardiovascular effects of intrarenal bradykinin. In a separate group of animals, chlorisondamine (7.5 mg/kg iv) completely blocked the increases in MAP and HR during intrarenal bradykinin (1 microgram/min). It is concluded that selective renal administration of bradykinin alters afferent renal nerve activity and that this results in hemodynamic changes consistent with efferent sympathetic activation.

Afferent Pathways↗
PubMed1985

Renal response to atrial natriuretic factor in conscious dogs with caval constriction.

Constriction of the thoracic inferior vena cava to decrease venous return and atrial filling markedly elevates plasma renin activity (PRA) and plasma aldosterone concentration (PAC) and produces chronic sodium retention and ascites in the dog. Infusion of a synthetic atrial natriuretic factor into conscious dogs with caval constriction and ascites at doses of 175 and 350 ng X kg-1 X min-1 for 30 min each produced striking increases (P less than 0.05) in creatinine clearance, diuresis, and kaliuresis but failed to increase urinary sodium excretion. Infusions of atrial natriuretic factor at these doses into conscious normal dogs, however, produced a striking increase in sodium excretion from 41 +/- 14 and 55 +/- 19 mu eq/min to 150 +/- 58 and 181 +/- 49 mu eq/min (P less than 0.05 for both values). Creatinine clearance and urine flow also increased in these normal dogs, but potassium excretion remained unchanged during the infusion periods. Atrial natriuretic factor produced parallel suppression (P less than 0.05) of the elevated levels of PRA and PAC in the caval dogs but failed to significantly decrease either PRA or PAC in the normal animals. Arterial pressure, heart rate, and PAH clearance were unchanged in both groups of dogs during infusion of atrial natriuretic factor. These results suggest that the pattern of renal electrolyte excretion elicited in response to the acute infusion of atrial natriuretic factor is dependent, at least partially, on the preexisting status of the renal tubules to facilitate sodium reabsorption and potassium excretion. The results also are consistent with the concept that atrial natriuretic factor might function to tonically inhibit the renin-angiotensin-aldosterone system.

Aldosterone↗
PubMed1986

Reduced osmotic and nonosmotic release of vasopressin after meclofenamate in the conscious dog.

Both in vivo as well as in vitro experiments suggest that prostaglandins (PG) may influence arginine vasopressin (AVP) release. Recent studies on conscious dogs have shown that cyclooxygenase inhibition with meclofenamate reduces basal AVP release as well as AVP release in response to hypoxia. The current experiments were performed in order to test whether PG synthesis inhibition affects osmotic- and nonosmotic-stimulated AVP release in a similar manner. Osmotic AVP release was tested by slowly infusing hypertonic saline intravenously in water-diuresing dogs and serially sampling plasma for AVP concentration. Experiments were performed both with and without meclofenamate (2 mg/kg and 2 mg X kg-1 X h-1 iv) pretreatment. AVP release to a comparable osmotic stimulus was greatly reduced after meclofenamate administration. Nonosmotic AVP release was tested by inducing systemic hypotension with an intravenous infusion of nitroprusside. Hypotension was associated with an increase in AVP concentration, which was partially blunted after meclofenamate administration. Experiments performed with only a saline vehicle administered showed no decrease in AVP release in response to comparable hypotension. The findings of these studies suggest that endogenous PG may be involved in both osmotic and nonosmotic AVP release in the conscious dog.

Animals↗
PubMed1986

Electrical stimulation in subfornical organ increases plasma vasopressin concentrations in the conscious rat.

Electrical stimulation in the subfornical organ (SFO) of conscious freely moving rats was found to increase plasma vasopressin concentrations from control values of 1.43 +/- 0.32 to poststimulation values of 22.32 +/- 4.9 pg/ml (P less than 0.01). Similar stimulation in immediately adjacent brain regions including the medial septum and hippocampal commissure caused no significant changes in plasma concentrations of this peptide hormone. These data indicate that activation of SFO neurons in conscious rats causes increased release of vasopressin from the posterior pituitary. Such data corroborate previous electrophysiological findings demonstrating that in anesthetized animals electrical stimulation in SFO results in increased excitability of antidromically identified vasopressin-secreting neurons in the supraoptic and paraventricular nuclei of the hypothalamus.

Animals↗
PubMed1986

Hemodynamics of hemorrhage in the conscious rat and chicken.

Hemodynamic responses to hemorrhage in conscious chicks (n = 10, 233 g) and rats (n = 10, 309 g) were compared. The animals were fitted with miniature pulsed Doppler aortic flow probes 2 days (chickens) or 5 days (rats) before catheterization, and the experiment began 1 (chickens) or 2 (rats) days later. Mean arterial pressure (MAP) and cardiac output (CO) were recorded continuously and simultaneously digitized to compute total peripheral resistance (TPR). MAP, CO, and TPR values were graphed on-line by a microcomputer and stored for later analysis. A 4-ml hemorrhage reduced MAP and CO by 25 and 43% in the rat, and 15 and 4% in the chickens, respectively. The fall in CO in the rat was due to reduction of stroke volume (SV) unlike the birds where SV was well maintained. TPR was elevated 65% in the rats and fell 13% in the chickens. The minimal fall in CO and SV in these conscious birds suggests that anesthetic agents used previously (i.e., urethane, paraldehyde, phenobarbital, and pentobarbital sodium) suppressed cardiac function. However, they do not account for the lack of a peripheral vascular response during hemorrhage. The chicken apparently maintains MAP by a volume regulating mechanism operating independently of peripheral vascular tone inasmuch as circulating fluid volume restitution is rapid and occurs without vasoconstriction. The rat maintains MAP through reflex cardiac and peripheral vascular responses which eventually may contribute to transvascular fluid loss and the ultimate collapse after prolonged hemorrhagic hypotension.

Animals↗
PubMed1987

Pulmonary depressor reflex elicited by capsaicin in conscious intact and lung-denervated dogs.

A pulmonary depressor reflex has been shown to be elicited in anesthetized cats, dogs, and rats by intravenous injection of capsaicin. The effects observed include apnea, hypotension, and bradycardia with some investigators reporting tachypnea following the apneic period. We investigated the response to a bolus injection of capsaicin (20 micrograms/kg) into the cephalic vein in 11 conscious beagle dogs. Five control dogs underwent sham thoracotomies, and six dogs underwent selective denervation of the lungs. A low dead-space latex rubber mask was used to monitor ventilation, and arterial blood pressure was obtained by catheterizing an exteriorized carotid artery. In four of the five control dogs the observed response was apnea concomitant with hypotension and bradycardia, followed by tachypnea. In five of the six lung-denervated dogs there was a slight tachypnea along with hypertension. It is concluded that the pulmonary depressor reflex can be elicited in conscious dogs by intravenous injection of capsaicin but is absent in lung-denervated dogs.

Animals↗
PubMed1988

Renal vascular response to combined hypoxia and hypercapnia in conscious rats.

Experiments were performed to test for a possible role of arginine vasopressin (AVP) in the renal vascular responses to the combination of hypoxia and varying levels of CO2 in the conscious rat. Animals were instrumented with pulsed Doppler flow probes on the left renal artery and with arterial and venous catheters. Renal blood flow (RBF) and mean arterial blood pressure (MABP) were determined in conscious, unrestrained rats under the following conditions: 1) hypocapnic hypoxia [arterial PO2 (PaO2) = 26 Torr; arterial PCO2 (PaCO2) = 21 Torr]; 2) isocapnic hypoxia (PaO2 = 34 Torr; PaCO2 = 36 Torr); 3) hypercapnic hypoxia (PaO2 = 42 Torr; PaCO2 = 57 Torr); and 4) room air control (PaO2 = 93 Torr; PaCO2 = 38 Torr). MABP fell from 104 +/- 2 to 83 +/- 5 mmHg during hypocapnic hypoxia but was unaffected by the other stimuli. RBF was significantly reduced by both hypocapnic and hypercapnic hypoxia and unchanged in the other protocols, whereas renal vascular resistance (RVR) was elevated only in the hypercapnic hypoxia group. Additional experiments were performed to test whether activation of V1-vasopressinergic receptors during hypoxia might mediate the observed changes in renal hemodynamics. Experiments were performed as before except that at the midpoint of hypoxic or room air exposure, 10 micrograms/kg of the specific V1 vasopressinergic antagonist d(CH2)5Tyr(Me)AVP was administered. However, administration of the V1 antagonist had no effect on the observed renal hemodynamic responses to hypoxia. Therefore, although intense chemoreceptor stimulation by hypercapnic hypoxia may increase RVR and decrease renal perfusion, these renal hemodynamic responses do not appear to be mediated by increased circulating levels of AVP.

Animals↗
PubMed1989

ANP and sodium excretion during acute baroreflex hypertension in conscious dogs.

The influence of an acute baroreflex hypertension elicited by common carotid occlusion (CCO) on plasma atrial natriuretic peptide (ANP) and renal sodium excretion was investigated in chronically instrumented, conscious foxhounds receiving a normal-sodium diet. CCO (n = 6) significantly increased mean arterial pressure (from 102 +/- 5 to 144 +/- 3 mmHg; P less than 0.01) and sodium excretion (from 82 +/- 10 to 133 +/- 9 mumol/min; P less than 0.05). No changes in plasma ANP and right atrial pressure were observed during the acute hypertension. In contrast, an acute 20% volume expansion (n = 7) corresponding to 1.8% of body weight raised right atrial pressure (from 1.3 +/- 1.2 to 5.8 +/- 1.2 cmH2O; P less than 0.01) and induced a sustained elevation of plasma ANP (from 39 +/- 8 to 67 +/- 16 pg/ml; P less than 0.05). The natriuresis in response to CCO was eliminated when renal perfusion pressure was regulated at the control level by a renal arterial cuff (n = 4); under these conditions, sodium excretion even tended to decrease during CCO (from 81 +/- 17 to 46 +/- 13 mumol/min; P less than 0.05). In conclusion, an increase in renal perfusion pressure and not an elevated ANP level is important in mediating the natriuresis during CCO in conscious dogs. These results imply that changes in plasma ANP are not essential for the induction and maintenance of a pressure natriuresis.

Acute Disease↗
PubMed1989

Volume expansion attenuates baroreflex sensitivity in the conscious nonhuman primate.

We examined the effect of intravascular volume expansion (VE) on the arterial baroreflex control of pulse rate (PR) in conscious, chronically instrumented monkeys tethered in their cages. A total of five monkeys was studied after surgical implantation of catheters in the descending aorta, the left atrium, and the internal jugular vein. Mean arterial blood pressure (MABP)-PR stimulus response curves were constructed by decreasing and increasing blood pressure with nitroprusside and phenylephrine, respectively. The data were analyzed with a regression analysis that generated a sigmoid curve and the maximum sensitivity (slope) of the curve. The data were obtained before and after VE with an isotonic isoncotic dextran solution equal to 20% of the estimated blood volume. After VE, the MABP-PR curve shifted to the right at the high blood pressures, and there was a significant decrease in the maximum sensitivity from 5.65 +/- 1.44 for control to 2.14 +/- 0.63 after VE (P less than 0.05). We concluded that VE attenuates the baroreflex control of heart rate in the conscious nonhuman primate.

Animals↗
PubMed1989

Effect of baroreceptor denervation on vasopressin and cortisol responses to angiotensin II infusion in conscious dogs.

Recent studies suggest that the pressor response to exogenous angiotensin II infusion may, through baroreceptor-dependent mechanisms, counteract the stimulatory effect of the peptide on vasopressin and adrenocorticotropic hormone (ACTH) secretion. To test this hypothesis, the effect of combined cardiac and sinoaortic baroreceptor denervation on the increases in plasma concentrations of vasopressin and cortisol (used as an index of ACTH secretion) produced by angiotensin II infusion was studied in conscious dogs. In eight intact dogs, 30-min angiotensin II infusions at 5, 10, and 20 ng.kg-1.min-1 increased mean arterial pressure from 108 +/- 5 to 126 +/- 5 mmHg, from 101 +/- 4 to 130 +/- 4 mmHg, and from 99 +/- 3 to 138 +/- 4 mmHg, respectively (P less than 0.001). Plasma cortisol concentration increased from 19 +/- 4 to 27 +/- 4 ng/ml, from 19 +/- 4 to 43 +/- 4 ng/ml, and from 19 +/- 4 to 71 +/- 6 ng/ml (P less than 0.01), and plasma vasopressin concentration increased from 2.2 +/- 0.3 to 3.1 +/- 0.3 pg/ml, from 2.3 +/- 0.3 to 3.5 +/- 0.4 pg/ml, and from 2.2 +/- 0.4 to 5.0 +/- 0.5 pg/ml (P less than 0.01). In five to six baroreceptor-denervated dogs, angiotensin II infusion produced increases in mean arterial pressure, plasma vasopressin concentration, and plasma cortisol concentration that were not consistently different from those in the intact dogs. These results demonstrate that baroreceptor denervation does not enhance the vasopressin or cortisol responses to angiotensin II infusion in conscious dogs.

Angiotensin II↗
PubMed1990

Vasopressinergic augmentation of cardiac baroreceptor reflex in conscious rats.

Experiments were performed on conscious, chronically instrumented rats to determine the contribution of V2-receptor activation in augmentation of cardiac baroreceptor reflex (BRR) sensitivity by arginine vasopressin (AVP). At least 1 wk before experimentation, rats were implanted with arterial and venous catheters, as well as with pulsed Doppler flow probes for measurement of cardiac output (CO). An initial set of experiments was performed to determine whether cardiac BRR sensitivity is enhanced by AVP in conscious rats. A series of pressor doses of either AVP or phenylephrine (PE) were administered on separate days (n = 8). The slope of pulse interval (PI) vs. mean arterial blood pressure (MABP) was determined for each experiment by linear regression and used as an index of cardiac BRR sensitivity. The slope of PI vs. MABP was greater in response to AVP than in response to PE in all animals studied. A separate group of animals (n = 7) received either a 40-min infusion of AVP (5 ng/min iv) or a specific V2-antagonist, d(CH2)5[DIle2,Ile4]AVP (20 micrograms/kg iv), 10 min before infusion of AVP. The responses of MABP, CO, and total peripheral resistance to AVP infusion were similar with and without V2-antagonism; however, the bradycardic response to AVP was less with V2-antagonist pretreatment. Furthermore, administration of V2-antagonist reduced delta PI/delta MABP in response to AVP infusion. Additional experiments were performed to test the effect of infusion of a specific V2-agonist, dVDAVP (5 ng/kg iv), on BRR-induced bradycardia in response to a series of pressor PE bolus doses.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Cardiac nerve blockade by infusion of procaine into the pericardial space of conscious dogs.

A technique was developed to produce acute, reversible cardiac nerve blockade (CNB) in the conscious dog by infusion of 2% procaine into the pericardial (PC) space. During CNB, reflex changes in heart rate (HR) in response to intravenous bolus injections of phenylephrine (100 micrograms) and nitroglycerin (300 micrograms) and the reflex tachycardia and hypotension after a 50-micrograms bolus injection of veratridine into the left atrium were abolished. In response to CNB, HR increased from 79 +/- 10 to 142 +/- 10 beats/min and mean arterial pressure (MAP) increased from 101 +/- 5 to 117 +/- 6 mmHg. Baseline values for plasma arginine vasopressin (AVP), plasma renin activity (PRA), and plasma norepinephrine (NE) were unchanged by CNB, but there was a small increase in plasma cortisol levels (1.4 +/- 0.3 to 2.3 +/- 0.3 micrograms/dl) during CNB. There was no significant change in the baseline levels of any of these hormones during PC infusion of 0.9% saline. To control for the possibility that procaine leaked into the systemic circulation, identical amounts of procaine were infused intravenously. Systemic administration of procaine caused a rise in MAP but had no effect on HR and did not alter plasma levels of AVP, PRA, NE, or cortisol. The relationship between plasma osmolality and plasma AVP, as well as the drinking response to a 60-min infusion of hypertonic NaCl, was unaltered by CNB. We conclude that PC procaine infusion is an effective technique for producing acute, reversible blockade of the cardiac nerves in the conscious dog.

Animals↗
PubMed1995

Biological actions and pharmacokinetics of C-type natriuretic peptide in conscious sheep.

C-type natriuretic peptide (CNP) is found in abundance in neural tissue and in endothelial cells of vascular tissue, where it may participate in the regulation of vascular tone. However, few studies have examined the metabolism and systemic actions of CNP in conscious animals. Accordingly, we investigated the hemodynamic, renal, and hormonal effects of intravenous CNP-22 administered at two doses (1 and 10 pmol.kg-1.min-1 as dose 1 and dose 10, respectively) in a vehicle-controlled study in normal conscious sheep (n = 8). Plasma CNP levels were raised from a mean baseline level of 2-3 pmol/l (detection limit) to plateau at 10 +/- 1.2 and 115 +/- 18 pmol/l during doses 1 and 10, respectively. Metabolic clearance rates were 3.15 +/- 0.39 and 2.48 +/- 0.36 l/min, respectively. The plasma half-life of CNP on termination of infusion was rapid (1.6 +/- 0.27 min). Dose 10 increased plasma guanosine 3',5'-cyclic monophosphate (P = 0.0002), reduced cardiac output by 18% (P = 0.01), but did not significantly affect mean arterial pressure. Similar suppression (15%) of cardiac output occurred during dose 1 (P = 0.078). Both doses were natriuretic. This study demonstrates that CNP is natriuretic in sheep and lowers cardiac output without significantly affecting arterial pressure. CNP may play an important role in the regulation of regional hemodynamics and fluid homeostasis.

Aldosterone↗
PubMed1997

Central injection of physostigmine attenuates exercise-induced pressor response in conscious cats.

The effects of intracerebroventricular administration of physostigmine, a cholinesterase inhibitor, on the cardiovascular responses evoked by static voluntary exercise were investigated using conscious cats. Four cats were trained to press a bar (200-650 g) with one forelimb for at least 20 s. The changes in mean arterial pressure (MAP), heart rate (HR), and developed force during the first five trials in 30 min by each individual cat were averaged, and a mean of the four values was then calculated. After the cats exercised for 30 min, either artificial cerebrospinal fluid (CSF) or physostigmine (5 micrograms) was administered intracerebroventricularly. Before physostigmine, exercise trials by the cats increased MAP and HR by 17 +/- 3 mmHg and 42 +/- 4 beats/min, respectively. Administration of physostigmine did not alter the resting MAP and HR but attenuated the MAP and HR responses to exercise (5-30 min postphysostigmine: MAP = 8 +/- 3 mmHg, HR = 25 +/- 7 beats/min; 30-60 min postphysostigmine: MAP = 4 +/- 3 mmHg, HR = 19 +/- 8 beats/min). Intracerebroventricular administration of CSF had no effect on the cardiovascular responses to static exercise. Pretreatment with the muscarinic antagonist, atropine (25 micrograms icv), blocked the attenuating effects of subsequent intracerebroventricular administration of physostigmine. These results demonstrate that stimulation of central muscarinic receptors attenuates the cardiovascular responses to static exercise by conscious cats. In addition, the present study suggests that there is no tonic effect of central muscarinic receptors on the cardiovascular responses to voluntary exercise.

Analysis of Variance↗
PubMed1998

Hemodynamic effects of acute stressors in the conscious rabbit.

Chronically instrumented, conscious rabbits were used to test the hypothesis that sensory stimulation with an air jet or oscillation produces differential hemodynamic changes that may be appropriate for an active or a passive behavioral response, respectively. Both stressors increased arterial pressure, central venous pressure, and hindquarters blood flow and produced visceral vasoconstriction. Neither stimulus altered hindquarters conductance. Although air jet increased heart rate and cardiac output, oscillation did not. The two stressors affected arterial baroreflex control of heart rate differently. Oscillation reset arterial pressure to a higher level with no change in heart rate maximum or minimum, whereas air jet reset both heart rate and arterial pressure to higher levels. Neither stressor affected baroreflex sensitivity. We conclude that the conscious rabbit shows at least two distinct cardiovascular responses when exposed to acute stressors. Air jet produces a cardiovascular response including tachycardia, which resembles the defense reaction and appears appropriate for active defense or flight. The response to oscillation, on the other hand, appears better suited for a passive response such as "freezing" behavior. During exposure to either stressor, the baroreflex is altered to allow simultaneous increases in heart rate and arterial blood pressure, but the sensitivity is maintained, allowing normal moment to moment control of heart rate.

Air Movements↗
PubMed1999

Sympathetic and cardiovascular actions of orexins in conscious rats.

The novel hypothalamic peptides orexin-A and orexin-B are known to induce feeding behavior when administered intracerebroventricularly, but little is known about other physiological functions. The renal sympathetic nerves play important roles in the homeostasis of body fluids and the circulatory system. We examined the effects of intracerebroventricularly administered orexins on mean arterial pressure (MAP), heart rate (HR), renal sympathetic nerve activity (RSNA), and plasma catecholamine in conscious rats. Orexin-A (0.3, 3. 0 nmol) provoked an increase in MAP (94.3 +/- 0.7 to 101.9 +/- 0.7 mmHg and 93.1 +/- 1.1 to 108.3 +/- 0.8 mmHg, respectively) and RSNA (28.0 +/- 7.0 and 57.9 +/- 12.3%, respectively). Similarly, orexin-B (0.3, 3.0 nmol) increased MAP (93.9 +/- 0.9 to 97.9 +/- 0.9 mmHg and 94.5 +/- 1.1 to 105.3 +/- 1.7 mmHg, respectively). Orexin-A and -B at 3.0 nmol also increased HR. In other conscious rats, a high dose of orexin-A and -B increased plasma norepinephrine. Plasma epinephrine only increased with a high dose of orexin-A. These results indicate that central orexins regulate sympathetic nerve activity and affect cardiovascular functions.

Animals↗