It has been established that naturally occurring pressor agents (adrenaline vasopressin and angiotensin ii) are all potent renal vasoconstrictors and, of these, vasopressin is the longer lasting and provides a back-ground of renal vasotonicity without which the kidney is unable to concentrate. The vasoconstriction affects particularly the renal outer cortical vessels and vasa recta and is associated with temporary oliguria or anuria (antidiuresis of varying degree). In association with renal outer cortical vasoconstriction there is active dilatation of the vessels supplying the adrenal gland and ovary as revealed by arteriography. Since vasopressin exerts a variable degree of renal vasotonicity according to circumstances, there appears to be an integrated feed-back system linking the neurohypophys's and hormonal responses by the adrenal and ovary through which tubular function is controlled. Since the vascular conduits between the renal artery and the adrenal gland and ovary reveal individual variation, the feed-back system induces responses which vary from modest to hyper-reactive which goes some way to explain the nature of individual responses. Taken in conjunction with other data, the evidence, strongly indicates that hormonal responses by the adrenal gland and the ovary are associated with increased blood flow. The integrated feed-back system assures that increased blood flow to the adrenal gland accompanies the appropriate signal for hormonal release. The widespread involvement of vasopressin in the systems of the body and particularly its influence on tubular function, it has been concluded, derives mainly from its vasopressor effect.
The presented evidence suggests that the medullary arteries of Flint represent the original blood supply of the chromaffin mass which migrates within the adrenal cortex during foetal life. The medullary arteries and venae comites constitute an independent vascular system within the adrenal gland.
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