AJP Legacy Watch the video to learn how APS reaches out to developing nations.
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol 206: 714-718, 1964;
0002-9513/64 $5.00
This Article
Right arrow Full Text (PDF)
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Webster, M. E.
Right arrow Articles by Gilmore, J. P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Webster, M. E.
Right arrow Articles by Gilmore, J. P.

Influence of kallidin-10 on renal function

Marion E. Webster 1 and Joseph P. Gilmore 1

1 Laboratory of Cardiovascular Physiology, National Heart Institute, National Institutes of Health, Bethesda, Maryland

The intrarenal infusion of kallidin-10 at 1–3 µg/min in the dog produces an increase in directly measured renal blood flow with no alteration in systemic blood pressure. Concomitant with the increase in blood flow, a diuresis is observed which is associated with substantial increases in sodium and chloride excretion but smaller increases in total solute and potassium excretion. Neither urinary pH nor free water changed consistently. The pattern of water and electrolyte secretion suggests that the observed changes are secondary to an increase in glomerular filtration rate, although an increase in endogenous creatinine or inulin clearance could not be detected. The contralateral kidney showed no changes during infusion of the decapeptide indicating the rapidity with which it is destroyed in vivo. The renal responses to acetylcholine mimic those produced by kallidin-10. These data, together with earlier observations showing that the kidney excretes both the proteinase, urinary kallikrein, and its hypotensive polypeptides, suggest that this enzyme system may contribute to renal blood flow regulation and to salt and water homeostasis.

Key Words: kallidin-10 and renal blood flow, water, and electrolyte excretion • renal response to vasodilator polypeptides dog kidney function

Submitted on August 16, 1963




This article has been cited by other articles:


Home page
J Clin PharmacolHome page
J. N. Sharma
Does the Kinin System Mediate in Cardiovascular Abnormalities? An Overview
J. Clin. Pharmacol., November 1, 2003; 43(11): 1187 - 1195.
[Abstract] [Full Text] [PDF]


Home page
Cardiovasc ResHome page
B. Nafz, K. Berger, C. Rosler, and P. B. Persson
Kinins modulate the sodium-dependent autoregulation of renal medullary blood flow
Cardiovasc Res, December 1, 1998; 40(3): 573 - 579.
[Abstract] [Full Text] [PDF]


Home page
Arch SurgHome page
A. S. Hermreck, R. A. Berg, J. R. Ruhlen, and R. I. MacArthur
Renal Response in Sepsis
Arch Surg, August 1, 1973; 107(2): 169 - 175.
[Abstract] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 1964 by the American Physiological Society.