Cardiovascular consequences of water deprivation in female Long Evans and Brattleboro rats.
Female Long Evans and Brattleboro rats were studied while water-replete and after water deprivation sufficient to cause hypovolaemia of similar degree in the two strains. A comparison was made of the blood chemistry and cardiovascular status in the two conditions, and the ability of the renin-angiotensin system, sympathoadrenal activity and (in Long Evans rats) vasopressin to influence blood pressure were assessed by pharmacological blockade of these systems. Under water-replete conditions there were significant differences between plasma variables in the two strains (Long Evans: vol., 3.67 +/- 0.07 ml/100 g b. wt., sodium, 142 +/- 0.3 mmol/l; osmolality, 290 +/- 1 mosmol/kg; Brattleboro: vol., 3.89 +/- 0.07 ml/100 g b. wt.; sodium 148 +/- 0.4 mmol/l; osmolality 304 +/- 2 mosmol/kg). Inhibition of the renin-angiotensin system (with captopril) had a slightly greater hypotensive effect in Brattleboro than in Long Evans rats. In both strains the hypotensive effects of captopril were enhanced markedly in the presence of pentolinium, and, under those conditions there was a vasopressin-dependent recovery of blood pressure in Long Evans rats that was absent in Brattleboro rats. Water deprivation caused a greater proportional reduction in body weight, and increase in plasma sodium and osmolality in Brattleboro than in Long Evans rats, although resting cardiovascular statuses were not markedly different. Despite Brattleboro rats having substantial hypernatraemia (156 +/- 1.0 mmol/l), that should have acted to inhibit renin release, they showed a profound hypotensive response to captopril that was not apparent in Long Evans rats. Thus, the absence of vasopressin in female Brattleboro rats severely affects cardiovascular adaptation to water deprivation. Comparison of the present results with published data obtained from male Long Evans and Brattleboro rats shows marked sex differences in the response to the same water deprivation protocol, and indicates that data obtained from males and females should not be cumulated.
Gardiner
S M
SM
Department of Physiology and Pharmacology, Medical School, Queen's Medical Centre, Nottingham, U.K.
Bennett
T
T
D000818:Animals; D001127:Arginine Vasopressin / Q000031:analogs & derivatives / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects; D002216:Captopril / Q000494:pharmacology; D002320:Cardiovascular Physiological Phenomena; D004573:Electrolytes / Q000097:blood; D005260:Female; D006339:Heart Rate / Q000187:drug effects; D010425:Pentolinium Tartrate / Q000494:pharmacology; D010953:Plasma Volume; D051381:Rats; D011910:Rats, Brattleboro / Q000502:physiology; D011919:Rats, Inbred Strains / Q000502:physiology; D014868:Water Deprivation / Q000502:physiology*
D004573:Electrolytes; D001127:Arginine Vasopressin; C025044:argipressin, beta-mercapto-beta,beta cyclopentamethylenepropionic acid(1)-; D010425:Pentolinium Tartrate; D002216:Captopril