Atrial, B-type, and C-type natriuretic peptides cause mesenteric vasoconstriction in conscious dogs.
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Cardiovascular responses were compared with equimolar infusions of B-type (BNP) and C-type (CNP) with atrial natriuretic peptide (ANP) in conscious, instrumented dogs. On separate days, each natriuretic peptide or vehicle was infused (intravenously) at step-up doses of 2, 5, 10, and 20 pmol. kg-1. min-1 (20 min each dose) to increase circulating levels of the infused peptide from approximately 2- to 20-fold. Like ANP, infusions of BNP caused dose-related increases (P < 0.05) in mesenteric vascular resistance, urine flow, natriuresis, and hematocrit (changes at highest doses were 60 +/- 9, 334 +/- 113, 313 +/- 173, and 12 +/- 2%, respectively). BNP also lowered (P < 0. 05) plasma renin activity (-43 +/- 11%) and arterial pressure (-10 +/- 3%). Effects of BNP were independent of reflex sympathetic activation, since autonomic ganglion blockade did not attenuate the responses. CNP infusions had little effect except to increase (P < 0. 05) mesenteric vascular resistance (27 +/- 10%) and plasma ANP (41 +/- 7%). Cardiovascular actions of BNP, like those of ANP, counteract the renin-ANG system and may protect the heart by lowering cardiac preload (venous return) and afterload (arterial pressure) while maintaining blood flow to extrasplanchnic regions. (+info)
Upregulation of immunoreactive angiotensin II release and angiotensinogen mRNA expression by high-frequency preganglionic stimulation at the canine cardiac sympathetic ganglia.
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The possible involvement of the local angiotensin system in ganglionic functions was investigated in the canine cardiac sympathetic ganglia. Positive chronotropic responses to preganglionic stellate stimulation at high frequencies, after intravenous administration of pentolinium plus atropine, were inhibited by the nonpeptide angiotensin AT(1) receptor antagonist forasartan or the angiotensin I-converting enzyme inhibitor captopril, whereas the rate increases elicited by the postganglionic stellate stimulation and norepinephrine given intravenously failed to be inhibited by these antagonists. The levels of endogenous immunoreactive angiotensin II, as determined by radioimmunoassay in the incubation medium of the stellate and inferior cervical ganglia, were increased after the high-frequency preganglionic stimulation of the isolated ganglia. The increment of the peptide was also antagonized by the pretreatment with captopril but not by a chymase inhibitor, chymostatin. The expression of angiotensinogen mRNA was observed in the stellate ganglion, adrenal, liver, and lung but not in the ovary and spleen. The expression of the mRNA in the stellate and inferior cervical ganglia increased after high-frequency preganglionic stimulation of the in vivo dogs for a period of 1 hour. These results indicate that an intrinsic angiotensin I-converting enzyme-dependent angiotensin system exists in the cardiac sympathetic ganglia, which is activated by high-frequency preganglionic stimulation. (+info)
Central orexin-A augments sympathoadrenal outflow in conscious rabbits.
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We determined the cardiovascular and neurohormonal responses to intracerebroventricular administration of orexin-A in conscious rabbits. Intracerebroventricular injection of orexin-A elicited dose-related increases in mean arterial pressure and renal sympathetic nerve activity. Peak values of mean arterial pressure and renal sympathetic nerve activity induced by intracerebroventricular injection of 100 pmol of orexin-A (14.0+/-0.7 mm Hg and 55.4+/-14.9%, respectively) were obtained at 40 and 25 minutes after injection, respectively. Plasma epinephrine and glucose concentrations were significantly increased at 60 and 90 minutes after intracerebroventricular injection of orexin-A (control versus 90 minutes; for epinephrine, 38.0+/-12.8 versus 167.5+/-42.5 pg/mL, P<0.01; for glucose, 6.66+/-0.18 versus 7.75+/-0.14 mmol/L, P<0.01). Plasma norepinephrine and insulin concentrations increased at 60 and 90 minutes but did not attain significant values. Intracerebroventricular injection of orexin-A also caused significant increases in plasma vasopressin concentrations. However, pretreatment with an intravenous injection of pentolinium (5 mg/kg), a ganglion-blocking agent, abolished these cardiovascular and neurohormonal responses. On the other hand, intravenous injection of the same dose of orexin-A (100 pmol) used in the intracerebroventricular experiment failed to cause any cardiovascular and renal sympathetic nerve responses. These results suggest that intracerebroventricular orexin-A acts in the central nervous system and activates sympathoadrenal outflow, resulting in increases in arterial pressure and plasma glucose levels in conscious rabbits. (+info)
Junction potentials in response to ortho- and anti-dromic stimulation of hypogastric nerve in mouse vas deferens.
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The interaction of the junction potentials in response to ortho- and antidromic hypogastric nerve stimulation in mouse vas deferens was studied, using an extracellular recording method. Ortho-dromic repetitive hypogastric nerve stimulation (10 Hz, 5 min) simultaneously depressed the amplitude of the junction potentials in response to both ortho- and anti-dromic hypogastric nerve stimulation (post-te-tanic depression). No time-lag in recovery from the post-tetanic depression was observed between the junction potentials recorded from two separate electrodes, indicating that the proximodistal axonal flow of available transmitter was not involved in the recovery process. Double shocks, with intervals from 10 msec to 1 sec, were applied to the hypogastric nerve. The junction potentials in response to ortho- and ortho-dromic or anti- and anti-dromic double shock were markedly facilitated. On the contrary, the junction potentials in response to ortho- and anti-dromic double shocks were not facilited. The findings indicate that facilitation of the junction potentials is produced by the impulses propagated in the same direction along the terminal axon and also that the origin of the facilitation may be at a pre-junctional site. (+info)
Central human cocaine- and amphetamine-regulated transcript peptide 55-102 increases arterial pressure in conscious rabbits.
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We determined cardiovascular and neurohormonal responses to intracerebroventricular administration of human cocaine- and amphetamine-regulated transcript (CART) peptide 55-102 in conscious rabbits. Intracerebroventricular injection of CART 55-102 elicited dose-related increases in mean arterial pressure and renal sympathetic nerve activity. Peak values of mean arterial pressure and renal sympathetic nerve activity induced by intracerebroventricular injection of 1 nmol of CART 55-102 (+5.0+/-2.6 mm Hg and +72.5+/-20.8%) were obtained 40 and 60 minutes after injection, respectively. Plasma epinephrine and glucose concentrations significantly increased 30 and 60 minutes after intracerebroventricular injection of CART 55-102 (control versus 60 minutes for epinephrine, 77.0+/-62.4 versus 1067.5+/-329.3 pg/mL, P<0.01; for glucose, 6.25+/-0.33 versus 11.57+/-0.93 mmol/L, P<0.01). Plasma norepinephrine concentrations also significantly increased at 30 minutes. Plasma insulin, vasopressin, and cortisol concentrations increased at 60 minutes but did not attain significant values. However, pretreatment with intravenous injection of pentolinium (5 mg/kg), a ganglion-blocking agent, eliminated these cardiovascular and neurohormonal responses. In contrast, intravenous injection of the same dosage of CART 55-102 (1 nmol) as that used in the intracerebroventricular experiment failed to cause any cardiovascular and renal sympathetic nerve responses. These results suggest that intracerebroventricular human CART 55-102 acts in the central nervous system and activates sympathoadrenal outflow, which results in increases in arterial pressure and plasma glucose levels in conscious rabbits. (+info)
Altered balance of main vasopressor and vasodepressor systems in rats with genetic hypertension and hypertriglyceridaemia.
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The precise role of nitric oxide (NO) in hypertension is still not fully understood, although this vasodilator system represents the main counterbalance of major pressor systems. The aim of our study was to determine the contributions of superoxide anions, the renin-angiotensin system (RAS), the sympathetic nervous system (SNS) and NO to the maintenance of blood pressure (BP) in Prague hereditary hypertriglyceridaemic (HTG) rats with genetic hypertension. Conscious chronically cannulated rats were subjected to the consecutive blockade of the RAS (losartan, 10 mg/kg), the SNS (pentolinium, 5 mg/kg) and NO synthase [N(omega)-nitro-L-arginine (L-NAME), 30 mg/kg]. Some additional rats were pretreated with tempol (a membrane-permeable mimetic of superoxide dismutase). A subsequent genetic study in HTG x Lewis F(2) hybrid rats (n=284) was designed to reveal potential associations of particular BP components with baseline BP. The progenitor study indicated that BP elevation was more pronounced in male than female HTG rats (as compared with normotensive Lewis controls). Higher BP in HTG rats was due to the increased residual BP (measured after combined RAS and SNS blockade) and the augmentation of BP responses to tempol or losartan. In contrast, BP responses to pentolinium or l-NAME were similar in all experimental groups. It should, however, be noted that the baseline BP of progenitor animals was correlated positively with both residual BP and the magnitude of the BP response to pentolinium, but not with BP response to L-NAME. Similarly, the baseline BP of F(2) hybrid rats was positively associated with residual BP, the BP response to pentolinium and the relative SNS contribution to BP maintenance [expressed as a percentage of baseline mean arterial pressure (MAP) values], as well as with the ratio of BP changes elicited by ganglion blockade and NO synthase inhibition (Delta MAP(pentolinium)/Delta MAP(L-NAME) ratio), reflecting the balance of main vasopressor and vasodepressor systems. Thus our studies, performed in progenitor and F(2) hybrid rats, revealed that changes in BP induced by L-NAME do not keep pace with the progressive augmentation of pentolinium-induced changes in BP occurring over a wide range of increasing BP. The altered balance between enhanced SNS-dependent vasoconstriction and unchanged NO-dependent vasodilation ('relative NO deficiency' in rats with high BP) might result in BP elevation in this form of genetic hypertension. (+info)
Hemodynamic response to ganglionic blockade with pentolinium during N2O-halothane anesthesia in man.
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Hemodynamic and blood-gas variables were studied before and after pentolinium tartrate administration in six patients anesthetized with nitrous oxide-halothane and maintained at PaCO2 35-40 torr. Measurements were made prior to induction of anesthesia; before and 10, 20, and 60 minutes after administration of pentolinium (0.3 mg/kg); 15 minutes after return of arterial blood pressure to control values. Mean arterial blood pressure (MAP) was significantly decreased at 20 (P less than 0.02) and 60 (P less than 0.001) minutes, in association with significant decreases in systemic vascular resistance (SVR) (P less than 0.05 and P less than 0.005). At 60 minutes MAP was significantly lower than that at 10 minutes (P less than 0.01). Cardiac output (CO) was increased (P less than 0.05) after 10 minutes secondary to a significant increase in heart rate. Neither variable changes significantly thereafter. CO and HR were significantly lower (P less than 0.01) 60 minutes after pentolinium than at 10 minutes; both returned to 10-minute values after intravenous administration of atropine. Changes in stroke volume (SV) and mean right atrial pressure (MRAP) were not significant. Whole-body O2 uptake (VO2) was not significantly altered by pentolinium. However, a substantial diminution of myocardial O2 consumption (MVO2) was deduced from a significant decrease in the heart rate-arterial systolic pressure produce (HR X ASP). Fifteen minutes after return of MAP to control levels, SVR was 11.5 per cent lower, while CO was still significantly higher (P less than 0.02) than control values. Following ganglionic blockade with pentolinium during halothane-N2O anesthesia, HR is a valuable index of changes in CO, while the HR X ASP index may be utilized to evaluate changes in MVO2. Assessment of myocardial performance during controlled hypotension is possible by the use of routinely available measurements. (+info)
Effects of some guanidine derivatives on neuromuscular and ganglionic transmission.
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The anticurare activity of some guanidine derivatives has been studied using the fowl sciatic nerve-gastrocnemius muscle preparation and the cat sciatic nerve-gastrocnemius and tibialis anterior muscle preparations. Among the compounds tested, and in decreasing order of potency, were NN-dimethylguanidine, N-methylguanidine, guanidine and N-aminoguanidine which antagonized or prevented tubocurarine or gallamine triethiodide-induced paralysis. None of the derivatives antagonized the effects of suxamethonium or decamethonium. NN-Dimethylguanidine, N-methylguanidine and guanidine antagonized or prevented the curare-like effects of magnesium without altering the activity of hemicholinium. At high doses NN-dimethylguanidine induced a decamethonium-like spastic paralysis in the fowl sciatic nerve-gastrocnemius muscle preparation. NN-Diethylguanidine, however, induced a tubocurarine-like flaccid paralysis. The derivatives possessing anticurare activity were also studied using the cat superior cervical ganglion-nictitating membrane preparation to check their possible effects against ganglionic blocking agents. Only guanidine antagonized or prevented the effects of hexamethonium, pentolinium and mecamylamine; it had no effect on the actions of pempidine and chlorisondamine. NN-Diethylguanidine was the only compound in the series to show a ganglionic blocking action. (+info)