vasopressin--1-(1-mercaptocyclohexaneacetic-acid)-2-(o--methyl-l-tyrosine)-8-l-arginine- and Hypotension

Hormonal systems such as vasopressin (AVP) and the renin-angiotensin-aldosterone system (RAS) have been reported to become activated during anesthesia and surgery. The purpose of this study was to examine the relative importance of AVP and angiotensin II (AII) in blood pressure control during isoflurane anesthesia in rats.. Rats were given an AVP V1-receptor antagonist (AVP-a, 10 microg kg(-1)), the AII receptor antagonist saralasin (SAR, 20 microg kg(-1) min(-1)) and hexamethonium (HEX, 10 mg kg(-1)) intravenously in random order, awake or anesthetized with isoflurane.. AVP-a had no effect on mean arterial pressure (MAP) in awake or anesthetized animals, but reduced MAP by 20.0+/-2.2% in the anesthetized rats which previously had been treated with SAR and/or HEX. SAR infusion had no effect on MAP when administered to conscious rats, but decreased MAP by 12.0+/-4.4% during anesthesia. Ganglionic blockade with HEX consistently lowered MAP in the conscious and anesthetized animals.. It is concluded that AVP contributes to the maintenance of blood pressure when the autonomic nervous system (ANS) and/or RAS are blocked during isoflurane anesthesia. SAR infusion leads to hypotension during anesthesia, but not in conscious rats. These findings indicate that AII is of importance for blood pressure maintenance during isoflurane anesthesia in rats, and that apparent pressor effects of AVP come into play when RAS and/or ANS are blocked.

Topics: Anesthesia, Inhalation; Anesthetics, Inhalation; Angiotensin II; Angiotensin-Converting Enzyme Inhibitors; Animals; Arginine Vasopressin; Autonomic Nervous System; Blood Pressure; Consciousness; Ganglionic Blockers; Hexamethonium; Hormone Antagonists; Hypotension; Infusions, Intravenous; Isoflurane; Male; Random Allocation; Rats; Rats, Sprague-Dawley; Renin-Angiotensin System; Saralasin; Vasoconstrictor Agents; Vasopressins

Intracerebroventricular (i.c.v.) choline (50-150 microg) increased blood pressure and decreased heart rate in spinal cord transected, hypotensive rats. Choline administered intraperitoneally (60 mg/kg), also, increased blood pressure, but to a lesser extent. The pressor response to i.c.v. choline was associated with an increase in plasma vasopressin. Mecamylamine pretreatment (50 microg; i.c.v.) blocked the pressor, bradycardic and vasopressin responses to choline (150 microg). Atropine pretreatment (10 microg; i.c.v.) abolished the bradycardia but failed to alter pressor and vasopressin responses. Hemicholinium-3 [HC-3 (20 microg; i.c.v.)] pretreatment attenuated both bradycardia and pressor responses to choline. The vasopressin V1 receptor antagonist, (beta-mercapto-beta,beta-cyclopenta-methylenepropionyl1, O-Me-Tyr2, Arg8)-vasopressin (10 microg/kg) administered intravenously 5 min after choline abolished the pressor response and attenuated the bradycardia-induced by choline. These data show that choline restores hypotension effectively by activating central nicotinic receptors via presynaptic mechanisms, in spinal shock. Choline-induced bradycardia is mediated by central nicotinic and muscarinic receptors. Increase in plasma vasopressin is involved in cardiovascular effects of choline.

Topics: Animals; Antidiuretic Hormone Receptor Antagonists; Arginine Vasopressin; Atropine; Blood Pressure; Cerebral Ventricles; Choline; Dose-Response Relationship, Drug; Heart Rate; Hemicholinium 3; Hormone Antagonists; Hypotension; Injections, Intraventricular; Male; Rats; Rats, Wistar; Spinal Cord; Spinal Cord Injuries; Time Factors; Vasopressins

This study investigated possible mechanisms for the hypotension produced by nitroprusside infusion in conscious dogs pretreated with a V1 vasopressin antagonist. The hypothesis that an action of vasopressin at V2-like receptors contributes to the hypotension was tested by comparing the effects of a V1 antagonist to the effects of a combined V1/V2 antagonist. Nitroprusside infusion produced dose-dependent decreases in arterial and atrial pressures. Larger decreases in pressures were produced in animals pretreated with either antagonist; however, the decreases in V1/V2-blocked dogs were not less than the decreases in V1-blocked dogs. These data suggest that V2-like actions of vasopressin do not contribute to the hypotensive effects of V1 blockade. A second hypothesis was that the greater hypotension was due to activation of a cardiac reflex to cause withdrawal of sympathetic tone, a decrease in peripheral resistance, and adrenal activation. Measurement of cardiac output revealed that the larger decreases in arterial pressure were due to larger decreases in total peripheral resistance. The hypotension was also associated with decreases in heart rate, unchanging plasma norepinephrine concentration, and increases in epinephrine concentration. These data are consistent with the hypothesis that the fall in pressure observed in dogs pretreated with a V1 antagonist is secondary to a decrease in peripheral resistance that is due at least in part to withdrawal of sympathetic tone.

Topics: Angiotensin II; Animals; Arginine Vasopressin; Blood Pressure; Cardiac Output; Deamino Arginine Vasopressin; Dogs; Dose-Response Relationship, Drug; Epinephrine; Female; Heart Rate; Hypotension; Injections, Intravenous; Male; Nitroprusside; Norepinephrine; Receptors, Angiotensin; Receptors, Vasopressin; Sympathetic Nervous System; Vascular Resistance; Vasopressins

We investigated possible interactions between arginine vasopressin (AVP) and endogenous opioid peptides during rapid hypotensive hemorrhage and subsequent opioid receptor blockade in conscious rabbits. Plasma AVP concentration did not change after normotensive hemorrhage but increased after hypotensive hemorrhage. Blockade of V1-AVP receptors (AVPX) did not affect prehemorrhage arterial pressure, heart rate, or hindquarter blood flow and vascular resistance. AVPX did not alter the hemodynamic response to hemorrhage or the blood loss required to reduce mean arterial pressure to less than 40 mmHg. However, hindquarter blood flow was higher and mean arterial pressure and hindquarter resistance lower after hypotensive hemorrhage in AVPX-treated animals. These differences were maintained after naloxone or saline injection. Naloxone increased mean arterial pressure and hindquarter resistance and decreased heart rate with or without AVPX. At 2 min postinjection, plasma AVP values were greater after saline than after naloxone. When naloxone's pressor response was reduced by alpha-adrenergic blockade, plasma AVP values were higher after naloxone than after saline. Thus AVP was not vital to maintenance of blood pressure during rapid normotensive hemorrhage or to the abrupt decrease in arterial blood pressure and resistance after rapid hypotensive hemorrhage. AVP release was important to spontaneous recovery from acute hypotensive hemorrhage but only of minor importance to naloxone's pressor response. Finally, AVP release appeared to be inhibited by endogenous opioids during acute hemorrhagic hypotension.

Topics: Animals; Arginine Vasopressin; Drug Interactions; Endorphins; Hemodynamics; Hemorrhage; Hypotension; Naloxone; Narcotic Antagonists; Rabbits; Rest

The interaction between vasopressinergic and prostanoid mechanisms in the control of cerebral hemodynamics in the conscious hypotensive newborn pig was investigated. Indomethacin treatment (5 mg/kg) of hypotensive piglets caused a significant decrease in blood flow to all brain regions within 20 min. This decrease in cerebral blood flow resulted from increased cerebral vascular resistances of 52 and 198% 20 and 40 min after treatment, respectively. Cerebral oxygen consumption was reduced from 2.58 +/- 0.32 ml.100 g-1.min-1 to 1.01 +/- 0.12 and 0.29 +/- 0.08 ml.100 g-1.min-1 20 and 40 min after indomethacin, respectively, in hemorrhaged piglets. Treatment with the putative vascular (V1) receptor antagonist [1-(beta-mercapto-beta, beta-cyclopentamethylene propionic acid-2-(O-methyl)tyrosine]arginine vasopressin (MEAVP) had no effect on regional cerebral blood flow, calculated cerebral vascular resistance, or cerebral metabolic rate either before or during hemorrhagic hypotension. However, decreases in cerebral blood flow and metabolic rate and increases in vascular resistance on treatment with indomethacin were blunted markedly in animals treated with MEAVP. These data are consistent with the hypothesis that the prostanoid system contributes to the maintenance of cerebral blood flow and cerebral metabolic rate during hypotension in the newborn pig, as reported previously, and implicate removal of vasopressinergic modulation by prostanoids as a potential mechanism for indomethacin-induced cerebral vasoconstriction in hypotensive newborn piglets.

Topics: Animals; Animals, Newborn; Arginine Vasopressin; Biomechanical Phenomena; Blood Pressure; Cardiac Output; Cerebrovascular Circulation; Hemorrhage; Hypotension; Indomethacin; Lypressin; Oxygen Consumption; Prostaglandins; Swine; Vascular Resistance; Vasopressins

In spontaneously hypertensive rats (SHR), the cessation of a 3-h intravenous infusion of arginine vasopressin (AVP, 8 mU/kg per min) resulted in a large and prolonged fall in arterial pressure (46 +/- 7.5 mmHg below basal levels). Pretreatment of SHR with the specific V1-receptor antagonist, [1-(beta-mercapto-beta, beta-cyclopentamethylene propionic acid), 2-(O-methyl)-tyrosine] AVP (d(CH2)5Tyr (Me)AVP, 8 micrograms/kg followed by 0.05 micrograms/kg per min) abolished the pressor response to AVP, and markedly reduced the subsequent hypotensive response following the cessation of the AVP infusion. The hypotensive response to AVP withdrawal was abolished also when phenylephrine hydrochloride (PE, 20 nmol/kg per min) elicited a blood pressure rise during the course of AVP infusion in rats with V1-receptor blockade. Finally, the concurrent administration of sodium nitroprusside (30 micrograms/kg per min) not only counteracted the pressure rise during AVP infusion, but also prevented the hypotensive response that normally accompanied the withdrawal of AVP. These findings demonstrate that neither V1-receptor activation nor blood pressure elevation alone was sufficient to generate a hypotensive response to the withdrawal of AVP; rather, both V1-receptor activation and a blood pressure elevation associated with the activation of these receptors were essential to the hypotensive response that followed the withdrawal of AVP in SHR.

Topics: Animals; Arginine Vasopressin; Blood Pressure; Heart Rate; Hypotension; Male; Nitroprusside; Phenylephrine; Premedication; Rats; Rats, Inbred SHR; Rats, Inbred Strains; Receptors, Angiotensin; Receptors, Vasopressin