By W. M. Manger, I. H. Page (auth.), Julian Rosenthal M.D. (eds.)
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Additional resources for Arterial Hypertension: Pathogenesis, Diagnosis, and Therapy
Since angiotensin II generation depends on the amount of renin released from the juxtaglomerular apparatus, efforts have been made to define abnormalities of factors controlling renin release and to classify patients with essential hypertension on the basis of plasma renin activity. The claim that hypertension in the high-renin patients is due to excessive vasoconstriction (which responds best to antirenin therapy), whereas in low-renin patients the elevated pressure is due to volume expansion (which responds best to diuretics) is controversial.
Kallidin and bradykinin increase sodium, potassium, and water excretion354 and, in addition, bradykinin is an arterial vasodilator in the kidney and elsewhere. Significantly decreased urinary excretion of kallikrein has been reported in patients with essential (GLANDULAR) ANGIOTENS/NOGEN ... ;t I KININASE I ----' ~ DEGRADATED PEPTIDES Figure 11. Diagram showing similarities of peptide generation by renin and kallikrein enzymatic actions. , ref 52, p 365 26 W. M. Manger, I. H. 224 An inverse relationship between urinary kallikrein concentration and blood pressure was also found in 601 children.
3. 4. 5. 6. 7. 8. 9. lO. 11. mal hypertensive rabbits. Acta Physiol Scand 72:298-309 Abboud FM (1974) Effects of sodium, angiotensin, and steroids on the vascular reactivity in man. Fed Proc 33:143-149 Ahrens RA (1974) Sucrose hypertension and heart disease; an historical perspective. Am J Clin Nutr 27:403-422 Aiken JW (1974) Effects of prostaglandin synthesis inhibitors on angiotensin tachyphylaxis in the isolated coeliac and mesenteric arteries of the rabbit. Pol J Pharmacol Pharm 26:217-227 Aiken JW, Vane JR (1973) Intrarenal prostaglandin release attenuates the renal vasoconstrictor activity of angiotensin.