Hind-limb/hind-quarter vascular resistance and blood flow changes: possible intrinsic renin--angiotensin system involvement.
For many years there was a general belief that the enzyme renin, having been secreted into the circulation by the kidney in response to appropriate stimuli, initially generates the inactive decapeptide angiotensin I in the bloodstream. This is then converted to the biologically active octapeptide angiotensin II by angiotensin converting enzyme on or near, vascular surface receptors both in the lungs and in the organs supplied by the systemic circulation. The results of various investigations have, however, latterly led to the conclusion that the overall system is widely distributed throughout the vasculature with the local intracellular formation of angiotensin II. In this review the reckoned intrinsic renin-angiotensin activity in hind-limb/hind-quarter is discussed with particular regard to the widespread use of radioimmunoassay, together with a consideration of other factors, more especially ACE inhibition, affecting the relevant regional vascular resistance and blood flow.
Duckworth
A J
AJ
Bristol-Myers Squibb Pharmaceuticals, Hounslow, UK.
Goodship
A E
AE
Kendall
H J
HJ
Osborn
E C
EC
D000818:Animals; D006614:Hindlimb / Q000098:blood supply*; D006801:Humans; D051381:Rats; D012039:Regional Blood Flow; D012084:Renin-Angiotensin System; D014655:Vascular Resistance