1. Urinary kallikrein, renal tissue kininogenase activity, and plasma kininogen were measured during the development of hypertension in rats, either with left renal artery clamped and contralateral kidney intact (Goldblatt 2-kidney) or removed (Goldblatt 1-kidney). Plasma urea, plasma volume and blood volume were also measured. 2. In Goldblatt 2-kidney rats, urinary kallikrein was not significantly different from that of sham-operated rats up to the 5th post-operative week even though at this time the Goldblatt 2-kidney animals were hypertensive. Urinary kallikrein started to decrease at week 8. Plasma kininogen was significantly elevated 5 and 10 weeks after surgery and returned to normal by week 15. No changes in renal tissue kininogenase activity were observed. Plasma urea and plasma and blood volumes were normal 5 weeks after, but significantly increased at 10 and 15 weeks after surgery. 3. In Goldblatt 1-kidney rats from the fifth week urinary kallikrein and renal kininogenase activity were significantly decreased compared with unilaterally nephrectomized rats, whereas plasma kininogen, plasma urea and plasma and blood volumes were significantly elevated. 4. These results show important differences in the kallikrein system between the Goldblatt 1-kidney and 2-kidney models of renovascular hypertension in rats.
1. Urinary kallikrein excreted by normal rats is significantly increased ( P < 0·001) 2 h after: (a) water loading, (b) water loading plus frusemide, 0·27 mmol (10 mg) per rat, (c) salt loading. In water-loaded rats, 5 i.u. of renin strikingly reduced kallikrein excretion ( P < 0·01) but considerably increased sodium excretion ( P < 0·001). 2. Renal kallikrein, measured by its kininogenase activity within 2 h of water loading, was significantly increased ( P < 0·05); after water loading and frusemide it was 40% decreased ( P < 0·001) and after salt loading it was reduced by approximately 50% ( P < 0·02). Renin did not change renal kallikrein. 3. Severely hypertensive (one-kidney) rats (blood pressure >150 mmHg) showed no increase of urinary kallikrein after water loading, although there was a marked natriuresis; in moderately hypertensive rats (blood pressure <150 mmHg) urinary kallikrein was only one-third of that observed in control normotensive rats, after an equal degree of water loading.
1. When the sino-aortic afferents are intact, desynchronized sleep causes a small decrease in the blood pressure, a vasodilatation in the mesenteric and renal beds, and a vasoconstriction in the external iliac bed. 2. After sino-aortic deafferentation desynchronized sleep causes a larger fall in the blood pressure, a greater vasodilatation in the mesenteric and renal beds, and a vasodilatation replaces the vasoconstriction in the external iliac bed. 3. The sino-aortic reflexes play an active role in controlling circulation during desynchronized sleep by opposing the centrally induced reduction in adrenergic sympathetic tone. This effect of sinoaortic reflexes is similar on both visceral and muscular vessels. In addition, the muscular bed, but not the visceral one, is regulated by a spinal reflex vasoconstriction mechanism which is apparent only when the sino-aortic reflexes are intact.