Renal effect of acute hypobaric pressure breathing in normal and diabetes insipidus rats.
The role of blood volume regulatory mechanisms located in the low pressure system in the control of urinary excretion was studied using hypobaric pressure breathing in normal and diabetes insipidus (Brattleboro strain with a congenital lack of vasopressin) rats. Rats were placed in an altitude simulator chamber for 4 h. A pump maintained pressure reduced to 701, 577 and 472 mbar simulating respectively altitude of 3,000, 4,500 and 6,000 m. In normal rats, hypobaric breathing induced an increase in urine flow, urinary urea and K+ excretion and urinary pH but did not significantly modify creatinine and Na+ excretion. In diabetes insipidus rats, hypobaric breathing produced oliguria and an decrease in urea, creatinine, Na+, K+, Cl- urinary excretions. Since acute hypobaric pressure breathing induced opposed effects in normal and Brattleboro rats, it is suggested that this kind of experimental procedure which increases intrathoracic blood volume elicits a diuretic response through an inhibition of vasopressin release. These experiments confirm the main role of vasopressin in the control of central blood volume.
D000399:Air Pressure; D000818:Animals; D001274:Atmospheric Pressure; D001810:Blood Volume; D002713:Chlorine / Q000652:urine; D003919:Diabetes Insipidus / Q000503:physiopathology* / Q000652:urine; D004195:Disease Models, Animal; D004231:Diuresis; D008297:Male; D009318:Natriuresis; D009846:Oliguria / Q000209:etiology; D010904:Pituitary Gland, Posterior / Q000502:physiology; D011188:Potassium / Q000652:urine; D051381:Rats; D011919:Rats, Inbred Strains; D014508:Urea / Q000652:urine; D014667:Vasopressins / Q000378:metabolism
D014667:Vasopressins; D002713:Chlorine; D014508:Urea; D011188:Potassium