Evidence and quantification of the vasopressin arterial pressure control system in the dog.

Cowley, Allen W.; Switzer, S. J.; Guinn, Meredith M.

doi:10.1161/01.res.46.1.58

Cited by 140 publications

(49 citation statements)

References 27 publications

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“…There was a significant inverse correlation between AVP levels and those of epinephrine and norepinephrine (figure 3), indicating that the more pronounced the depletion of catecholamines, the more the release of AVP was stimulated. This could partly be attributed to hypotension per se acting as a stimulus for secretion of AVP 10 and partly to removal of the attenuating or inhibitory influence of catecholamines on the secretion of AVP. 8 ' n~13 In the anephric model, the participation of AVP in maintaining blood pressure after chemical sympathectomy was far more important, as shown by both the excessively high plasma AVP levels and the magnitude of blood pressure fall (average 40 mm Hg) after injection of the AVP antagonist ( fig.…”

Section: Discussionmentioning

confidence: 99%

Interaction of the sympathetic nervous system with vasopressin and renin in the maintenance of blood pressure.

Gavras¹,

Hatzinikolaou²,

North³

et al. 1982

Hypertension

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SUMMARY To evaluate the partial contributions and interaction of three vasopressor systems in blood pressure maintenance, nephrectomized rats and rats with intact kidneys were submitted sequentially to catecholamine depletion, elimination of vasopressin's vasoconstrictor action, and (for those with kidneys in situ) angiotensin blockade. Catecholamine depletion decreased blood pressure and stimulated vasopressin levels in all rats, but significantly more so in the anephric ones. Subsequent injection of an antagonist to the vasopressor effect of vasopressin produced a lasting fall of blood pressure in anephric rats, but only transient fall in those with intact kidneys. Infusion of teprotide -an angiotensin converting enzyme inhibitor -in the latter animals also produced transient blood pressure fall, but if this were followed by injection of the vasopressin antagonist, the pressure remained low for several hours. Blood pressure levels were closely correlated with those of plasma catecholamines throughout these maneuvers. Catecholamine levels were inversely correlated with those of plasma vasopressin, which were far greater in anephric rats through both stimulation and accumulation. Plasma renin activity was increasingly stimulated by falling blood pressure after each maneuver in rats with intact kidneys. Thus, it appears that in the resting state the sympathetic nervous system is more involved in the maintenance of blood pressure, whereas vasopressin and renin are important backup mechanisms. The present experiments were designed to evaluate the contribution of each one of these three vasopressor systems to the maintenance of normal blood pressure. Catecholamine depletion and bilateral nephrectomy were intended to produce conditions comparable -albeit extreme -to those likely to be encountered in the therapy of human hypertension, e.g., treatment with sympatholytic agents and advanced renal failure. Under these conditions, we studied the interaction and relationships of catecholamines, vasopressin, and the renin-angiotensin system.

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Section: Discussionmentioning

confidence: 99%

Interaction of the sympathetic nervous system with vasopressin and renin in the maintenance of blood pressure.

Gavras¹,

Hatzinikolaou²,

North³

et al. 1982

Hypertension

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“…Hypotensive hemorrhage in dogs and monkeys can acutely increase plasma levels to 100 to 1,000 pg/mL. 29,44,53 However, during prolonged hemorrhagic shock in dogs, an initial increase in plasma vasopressin levels to 319 pg/mL was followed by a decrease to 29 pg/mL. 45,46 Similarly, acute endotoxin-induced shock results in extremely high levels of vasopressin (Ͼ 500 pg/mL in dogs and Ͼ 300 pg/mL in baboons).…”

Section: Vasopressin Levels In Shockmentioning

confidence: 99%

“…64,65 Supraphysiologic plasma vasopressin levels of about 50 pg/mL must be attained before a significant increase in mean arterial BP is achieved in normal dogs and humans. 53,66 However during hypovolemia, vasopressin helps maintain arterial BP. V1-receptor antagonists administered to animals subjected to hemorrhage cause hypotension, 10,67 and vasopressin levels rise during hypotension 22,68 ; therefore, vasopressin is an important hormone in preserving perfusion pressure during hemorrhage.…”

Section: Vasoconstrictor Effectsmentioning

confidence: 99%

Physiology of Vasopressin Relevant to Management of Septic Shock

Holmes

Patel

Russell

et al. 2001

Chest

538

395

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“…The fact that has recently stimulated research in this aspect of AVP was the development of AVP receptor antagonists by Manning's team. 1 -2 By using some of these antagonists, several investigators were able to demonstrate a pressor role for AVP in normotension, 3 in maintaining blood pressure during hypovolemia, 4 -5 and in certain types of experimental hypertension. 6 Our own earlier studies with the compound d(CH 2 ) 5 -0-(Me)Tyr-AVP, revealed that the pressor function of AVP was most apparent on salt loading, 7 -8 was closely interrelated to those of the RAS and the SNS, and was maximized when the other two were impaired or eliminated.…”

mentioning

confidence: 99%

Pressor systems in hypertension and congestive heart failure. Role of vasopressin.

Gavras

1990

Hypertension

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Elevated peripheral vascular resistance, which characterizes hypertension and congestive heart failure (the latter regardless of absolute blood pressure level) is maintained to a large extent by the combined effects of three major neurohormonal pressor mechanisms: the renin-angiotensin system, the sympathoadrenal system, and arginine vasopressin. Blockade of one of these mechanisms may lead to compensatory stimulation of the others, thus offsetting in part the hemodynamic benefits of a specific intervention. Combination therapy, designed to attack all three systems (with use of an angiotensin converting enzyme inhibitor, a sympathetic blocker such as clonidine, and an antagonist of the vasopressor action of vasopressin), may help in the treatment of such cases. To illustrate this strategy, two experimental studies, one case of malignant hypertension, and one case of congestive heart failure are presented. (Hypertension 1990;16:587-593) I t is generally recognized that a given level of arterial blood pressure is maintained to a large extent by the combined effects of three major neurohormonal pressor mechanisms: the renin-angiotensin system (RAS), the sympathetic nervous system (SNS), and arginine vasopressin (AVP). Several lines of experimental and clinical work over the years have demonstrated the participation of any one of these pressor mechanisms in the development and maintenance of various types of hypertension-or even in the maintenance of normotension. The first two, the RAS and the SNS, have been extensively investigated, and their research has yielded invaluable new treatments for hypertension and congestive heart failure that have now become part of the routine therapeutic armamentarium. The third, AVP, has long been known as the antidiuretic hormone that regulates fluid homeostasis. Only recently has it become the focus of experimental and clinical investigation as an important vasopressor mechanism with potential relevance in clinical situations characterized by elevated systemic vascular resistance such as hypertension and congestive heart failure. The fact Our own earlier studies with the compound d(CH 2 ) 5 -0-(Me)Tyr-AVP, revealed that the pressor function of AVP was most apparent on salt loading, 7 -8 was closely interrelated to those of the RAS and the SNS, and was maximized when the other two were impaired or eliminated.910 These findings were confirmed and amplified subsequently by other investigators. 1112 Because AVP analogues are known to have species-specific action, we set out to investigate the possible relevance of these findings in human pathophysiology. We took the above mentioned Vi antagonist through the various steps of pharmacological development to obtain an investigational new drug (IND) exemption number from the Food and Drug Administration (FDA) for its use in humans. 13 With this new pharmacological tool, we attempted to clarify the interaction of the three pressor systems-the RAS, the SNS, and AVP-in human hypertension and congestive heart failure. The following two case...

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Evidence and quantification of the vasopressin arterial pressure control system in the dog.

Cited by 140 publications

References 27 publications

Interaction of the sympathetic nervous system with vasopressin and renin in the maintenance of blood pressure.

Interaction of the sympathetic nervous system with vasopressin and renin in the maintenance of blood pressure.

Physiology of Vasopressin Relevant to Management of Septic Shock

Pressor systems in hypertension and congestive heart failure. Role of vasopressin.

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