Vascular Effects of Arginine Vasopressin during Fluid Deprivation in the Rat

The roles of the sympathetic nervous system, angiotensin II, and arginine vasopressin in the cardiovascularrenal responses to nitric oxide synthesis inhibition were examined in eight conscious dogs equipped with arterial and venous catheters and a nonoccluding bladder catheter. Nitric oxide inhibition was achieved by intravenous infusion of TV°-nitro-Larginine methyl ester (L-NAME) at 37.1 nmol/kg per minute for 140 minutes in the control group. The same dogs, after a 1-week recovery, were pretreated for 2 days with either prazosin for a, blockade, prazosin plus propranolol for a, plus /3 blockade, L-158,809 for angiotensin receptor blockade, or d(CH 2 )Tyr(Me)arginine vasopressin for vasopressin-V, blockade, and the L-NAME infusion was repeated. After 140 minutes of L-NAME infusion into the control group, mean arterial pressure and renal vascular resistance had increased 16% and 71%, and renal blood flow, glomerular filtration rate, urine flow, and urinary sodium excretion had decreased 33%, A number of recent studies have shown that nitric oxide (NO) synthesis inhibition causes both L. acute and chronic increases in arterial pressure. 18 In addition, several studies have shown that administration of the NO synthesis inhibitor Af G -nitro-L-arginine methyl ester (L-NAME) causes acute 9 and chronic 12 renal vasoconstriction in rats. Several investigators have also shown that inhibition of NO synthesis enhances the vasoconstrictor actions of a number of neurohumoral systems.1013 Therefore, it is conceivable that some of these pressor and renal vasoconstrictor effects of NO synthesis inhibition could be mediated by other neurohumoral factors.NO synthesis inhibition in anesthetized rats has been shown to cause at least a short-term increase in renal nerve activity.10 Also, application of L-NAME to isolated afferent arterioles amplified the acute vasoconstrictor effects of angiotensin II (Ang II).11 In addition, acute NO synthesis inhibition amplified the pressor effects of arginine vasopressin (AVP).12 -13 Therefore, NO release may oppose the effects of several vasoconstrictor systems.A recent study in anesthetized rats showed that the pressor and renal vasoconstrictor effects of L-NAME were not attenuated during individual or combined blockade of all the major vasoconstrictor systems.5 However, another study in anesthetized rats showed that 16%, 61%, and 64%, respectively. The decrement in renal blood flow and glomerular filtration during L-NAME administration was unaffected by any of the neurohumoral blockers. During V, blockade L-NAME resulted in only a 3% increase in arterial pressure, attenuation of the renal vascular resistance response, and almost total elimination of the decrease in urine flow. During angiotensin blockade the L-NAME-induced increase in arterial pressure was markedly attenuated, and the decrease in urinary sodium excretion was attenuated in the a, plus f3 blockade group. In conclusion, short-term renal and cardiovascular effects of nitric oxide synthesis inhibition in conscious dogs...

Section: Discussionmentioning

confidence: 61%

Mechanisms involved in the cardiovascular-renal actions of nitric oxide inhibition.

Manning

Williamson

1994

“…24 It should also be noted that the MAP measured by this method is significantly lower than the MAP recorded in studies using other direct measurements in restrained animals. 15 28 the plasma renin activity of Brattleboro rats was found to be significantly higher than in agematched Long-Evans rats. The difference may either represent a compensatory mechanism counter-balancing the absence of the pressor action of vasopressin or it may be a consequence of the volume contraction of Brattleboro rats.…”

Section: Discussionmentioning

confidence: 76%

Chronic arterial and venous catheterization of conscious, unrestrained rats.

Fejes-Tóth¹,

Náray-Fejes-Tóth²,

Ratge³

et al. 1984

GEZA FEJES-T6TH, ANIK6 NARAY-FEJES-T6TH, DIETER RATGE, AND JURGEN C. FROLICH SUMMARY A method is described for implanting arterial and venous cannulas in rats that requires only minor surgery. Catheters are introduced into the abdominal aorta through the ventral tail artery and into the vena cava through a lateral tail vein. The wounds are covered with an acrylic cuff and the catheters are brought out through a stainless steel spiral connected to the cuff and then attached to top of a metabolism cage used to house the rat. This method makes possible continuous access to the catheters in undisturbed, mobile animals. Using this model we compared mean arterial pressure, heart rate, plasma renin activity, and plasma catecholamine levels in freely moving Long-Evans rats and in Brattleboro homozygous rats. (Hypertension 6: 926-930, 1984) KEY WORDS • chronic vascular catheters • blood pressure • Brattleboro rat • plasma renin activity • plasma catecholamines A LTHOUGH most of our present knowledge in animal physiology comes from experiments performed on anesthetized animals or from in vitro studies, the utility of these preparations is often curtailed when highly complex neural or hormonal regulatory mechanisms are investigated. Basal secretion rates and plasma levels of most hormones are drastically influenced by anesthesia and surgical trauma,'" 3 and even simple handling of animals may have profound effects. The effect of general anesthesia on mean arterial pressure (MAP) and cardiovascular control mechanisms is well established, 6 and even kidney function, which was generally regarded to be immune to these interventions, has recently been found to be markedly depressed during and following general anesthesia and surgical stress.7 " 9 Although methods have been developed to study larger laboratory animals under relatively unstressed conditions, such methods have not been generally adopted for the rat.We describe a simple, chronic rat preparation that makes possible intravenous infusions, continuous monitoring of MAP and heart rate (HR), and repeated blood sampling in freely moving animals. Since vasopressin has been suggested to be involved in the regulation of blood pressure, 10 we have also compared the resting MAP of the Brattleboro rat suffering from hereditary diabetes insipidus" with the blood pressure of the normal Long-Evans rat from which the Brattleboro rat has been derived. Materials and Methods A slightly conic protecting cuff with a bulging middle portion was made from a rod of plexiglass on a lathe (Figure 1). A hole was bored into the middle portion of the cuff, and perpendicular to it a longitudinal slit was made. A 3 mm diameter stainless steel spiral, which had been previously stretched to 105% of its original length to render it more flexible, was glued into the cuff with epoxy. The first few centimeters of the spiral were fortified by surrounding it with a 4 mm diameter spiral. Two 55 cm long PE-10 tubings (ClayAdams, Parsippany, New Jersey) were fed through the spiral, the proximal ends of th...

“…42 This dose completely prevented the pressor response to 10 mM of exogenous vasopressin in every animal studied. The animals were then infused with CaCl 2 (n = 7) or NaCl (n = 5), and MAP was measured, as described before.…”

Section: Role Of Vasoconstrictive Hormones On the Pressor Response Tomentioning

confidence: 86%

Mechanism of acute hypercalcemic hypertension in the conscious rat.

Berl¹,

Levi²,

Ellis³

et al. 1985

SUMMARY Acute hypercalcemia in the conscious, unanesthetized rat, achieved by a 30-minute infusion of CaCl 2 (serum calcium level, 12.8 ± 0.6 mg/dl) resulted in significant elevation of mean arterial pressure (from 112 ± 2 mm Hg to 129 ± 3 mm Hg, p < 0.001). This pressor response was associated with a significant increase in systemic vascular resistance, from 0.45 ± 0.02 mm Hg/(ml/min)/kg body weight to 0.50 ± 0.02 mm Hg/(ml/min)/kg body weight (p < 0.05), but it caused no alteration in cardiac index. The pressor response to acute hypercalcemia does not appear to be mediated by vasopressor hormones or attenuated by vasodepressor hormones since inhibition of the renin-angiotensin system (nephrectomy), catecholamines (central and peripheral 6-hydroxydopamine), vasopressin (vascular antagonist), prostaglandins (indomethacin), and parathyroid hormone (parathyroidectomy) did not significantly alter the pressor response to infusion of CaCI 2 in spite of similar serum calcium levels in all groups of animals. Rather, the pressor response to acute hypercalcemia seems to be mediated by a direct action of calcium ion on smooth muscle and perhaps myocardial cell contractility, since pretreatment with the calcium channel blockers verapamil or nifedipine blocked the pressor response to acute hypercalcemia. (Hypertension 7: 923-930, 1985)