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

1. High-sodium intake may increase blood pressure and diabetes is a salt-sensitive condition. In the present study, we evaluated cardiovascular changes and their neurohumoral mechanisms in streptozotocin (STZ)-diabetic rats that underwent chronic salt loading. 2. We studied male Wistar rats (150-280 g) 14 days after the injection of either STZ (50 mg/kg, i.v.; D; n = 18) or citrate buffer (C; n = 16). After the induction of diabetes, animals were maintained for 14 days with free access to standard rat chow and tap water (C and D groups) or 1% NaCl solution (C-S and D-S groups). We conducted two experiments. Experiment 1 consisted of basal arterial pressure (AP) measurement (30 min) followed by the evaluation of AP responsiveness to phenylephrine and sodium nitroprusside. One day later, with the rats anaesthetized, a blood sample was collected to test for glycaemia, plasma angiotensin-converting enzyme (ACE) activity and renin. Kidneys were removed for the determination of tissue ACE activity. Experiment 2 comprised 24 h urine collection followed by 3 days of cardiovascular records, which consisted of a 30 min basal AP measurement, followed by injection of blockers of the vasopressin system, the renin-angiotensin system (RAS) and the sympathetic system. Basal haemodynamic data, baroreflex evaluation and AP responses to blockade of the vasopressin system with vasopressin V(1) receptor antagonist (aAVP; 10 mg/kg, i.v.), the RAS by losartan (10 mg/kg, i.v.) and the sympathetic system by hexamethonium (20 mg/kg, i.v.) were determined. 3. Glycaemia was similar between C and C-S (P = 0.612) and between D and D-S (P = 0.552), but higher in diabetic compared with non-diabetic rats (P < 0.0001). The D-S rats had an increment of 24% in mean AP compared with D (120 +/- 4 vs 97 +/- 2 mmHg, respectively; P = 0.0001), which was not seen in C-S compared with C rats. A positive association was noted between urinary sodium and mean AP (r = 0.37; P = 0.04). Plasma renin was undetectable in D-S rats. The response to acute drug blockade of vasopressin and the RAS was similar among groups, but hexamethonium elicited a more pronounced decrease in AP in D-S compared with D rats (P = 0.001). 4. The main neurohumoral mechanisms of salt-induced cardiovascular changes in STZ-diabetes are increased sodium and vascular sensitivity to adrenergic stimuli, which act in combination to produce a final result of higher AP levels, a finding not observed in control rats. Baroreflex derangemen

Topics: Angiotensin II Type 1 Receptor Blockers; Animals; Arginine Vasopressin; Baroreflex; Blood Glucose; Blood Pressure; Body Weight; Diabetes Mellitus, Experimental; Ganglionic Blockers; Heart Rate; Hematocrit; Hexamethonium; Hormone Antagonists; Hypertension; Kidney; Losartan; Male; Nitroprusside; Organ Size; Peptidyl-Dipeptidase A; Phenylephrine; Rats; Rats, Wistar; Renin; Renin-Angiotensin System; Sodium Chloride, Dietary; Sympathetic Nervous System; Vasoconstrictor Agents; Vasodilator Agents; Vasopressins

To assess the role of the vomeronasal organ (VNO) in the dependence of social recognition on vasopressinergic transmission, vomerectomized rats were compared to intact and castrated male rats. Removal of the VNO significantly decreased the duration of social investigation and temporarily impaired social recognition. In contrast to sham-operated animals and non-operated animals, lesioned rats were no longer responsive to the blocking effect of the antagonist of the vasopressor receptors of vasopressin (dPTyr(Me)AVP, 30 micrograms/kg subcutaneously) on social recognition. Consequently, VNO-lesioned rats behave like castrates, in spite of the lack of effect of removal of the VNO on plasma testosterone levels. These results suggest that androgen-dependent vasopressinergic neurons are part of the VNO pathway and that the VNO system is important for processing and storage of socially relevant information in male rat.

Topics: Animals; Arginine Vasopressin; Body Weight; Dose-Response Relationship, Drug; Male; Nasal Septum; Orchiectomy; Rats; Rats, Wistar; Reference Values; Social Behavior; Testosterone

The role of arginine vasopressin (AVP) in blood pressure regulation in humans and animals is still controversial. The present study was designed to investigate the effects of AVP on blood pressure and the excretion of sodium and prostaglandin (PG) E2 in rabbits. AVP dissolved in 0.01 M acetic acid was infused subcutaneously at a rate of 0.86 ng/kg/min with a miniosmotic pump into 12 New Zealand white rabbits (2.7-3.4 kg), while 10 controls were given vehicle alone. AVP infusion resulted in a 3.5-fold rise in the level of plasma AVP (21.8 +/- 4.4 (SEM) pg/ml) as compared with controls, associated with a significant decrease in the urine volume and urinary excretion of sodium. The PGE2 excretion was increased 1.8-fold after AVP infusion. In the chronic AVP-infused group, blood pressure was not significantly increased, but the acute vascular response to AVP was significantly attenuated without any changes in the vasopressor response to angiotensin II. Preadministration of V1-antagonist completely abolished the vasopressor action of AVP, but not that of angiotensin II, in either group. These results suggest that circulating AVP within physiological range of concentrations may stimulate renal PGE2 synthesis and attenuate the vascular response through vascular V1 receptors without affecting the baroreflex, which may be attenuated through V2 receptors.

Topics: Angiotensin II; Animals; Arginine Vasopressin; Blood Pressure; Body Weight; Dinoprostone; Drinking; Heart Rate; Kidney; Potassium; Rabbits; Renin; Sodium