Haemodynamic and Humoral Consequences of Chronic Infusion of Vasopressin in Conscious Rats

Abstract

1. To determine the long-term haemodynamic and humoral effects of arginine vasopressin (AVP), a chronic intravenous infusion of AVP was performed in conscious Wistar normotensive rats. 2. AVP (1, 10, 50 or 100 ng/h) or saline as a vehicle control was infused continuously into the right jugular vein at a rate of 1 microL/h using an osmotic minipump for 7 days. 3. As a result, significant elevations of systolic blood pressure were observed in association with increases in plasma AVP concentration. Significant decreases in heart rate were observed during infusion of 100 ng/h of AVP. Mean arterial pressures measured directly on the sixth day of infusion were significantly higher in the rats given 50 ng/h (125 +/- 3 mmHg) or 100 ng/h (125 +/- 2 mmHg) compared with control rats (117 +/- 2 mmHg). Intravenous injection of the V1 antagonist, d(CH2)5Tyr(Me)AVP, significantly reduced the elevated mean arterial pressure induced by 50 or 100 ng/h of AVP (-7 +/- 4 and -11 +/- 2 mmHg, respectively). Plasma renin and norepinephrine concentrations were not affected by AVP infusion, while plasma epinephrine concentration was lower in the rats given 100 ng/h of AVP. Intravenous infusion of AVP did not alter bodyweight, serum electrolytes or osmolality. 4. These results suggest that AVP has a long-term pressor effect which is attributable to its vasoconstrictor action in conscious rats.

Oxytocin Attenuates Stress-Induced c-fosmRNA Expression in Specific Forebrain Regions Associated with Modulation of Hypothalamo–Pituitary–Adrenal Activity

“…This suggests that the functional effects are highly peptide selective, despite the fact that vasopressin has a high affinity for the rat brain oxytocin receptor (Audigier and Barberis, 1985). This functional selectivity is unlikely to arise from a degradation of vasopressin in the Alzet pump in vivo, because studies of the cardiovascular effects of vasopressin have shown that Alzet minipumps can sustain delivery of biologically active vasopressin over a 7 d period (Tsuchihashi et al, 1993). Second, although we cannot completely exclude a possible direct inhibition of the pituitary-adrenal axis attributable to oxytocin leakage from the ventricular system, this is unlikely because all evidence suggests that circulating oxytocin acts to stimulate rather than inhibit ACTH release at the pituitary (Antoni et al, 1983;Gibbs et al, 1984;Rivier and Shen, 1994).…”