Interrelationship of Electrolytes, Juxtaglomerular Cells and Hypertension

The Goldblatt memorial lecture. Part I: Experimental renovascular hyptertension.

“…Thus, in the sodium-depleted animal, the enhanced ability to release renin makes the reninangiotensin system a very effective pressure regulator during volume depletion; in high-salt states it plays little role in regulation of pressure. In contrast to the above observations, Rocchini et al 46 have shown that the blood pressure response to a similar degree of hypotension in the carotid sinus (25 mm Hg) produced by constricting van Leersum loops in the trained dog is higher in the salt-replete animal, and is attenuated by 50% in the salt-depleted dog. Figure 5 provides a quantitative comparison of the effectiveness of the renin-angiotensin system and the carotid sinus reflex in the elevation of blood pressure in the sodiumdepleted animal (left) and sodium-replete dogs (right).…”

“…Conventional wisdom might suggest that the carotid sinus reflex would be more important in the regulation of blood pressure during volume depletion, but, as DeChamplain et al 43 have reported, the turnover of norepinephrine is markedly depressed by sodium depletion even though tissue norepinephrine content is greater than in the sodium-replete animal. Hence, it is not surprising that, in the volumedepleted dog, Rocchini and co-workers 46 found that the blood pressure dose-response curve to tyramine, a drug that releases norepinephrine from nerve terminals, was shifted to the right of that obtained in the sodium-replete dog; that is, a higher concentration of tyramine was required to produce an equivalent rise in blood pressure. The vascular responsiveness to norepinephrine was unchanged by varying sodium chloride intake.…”

Cellular control of renin secretion

“…Experimental observations and theoretical considerations led to the suggestion that the baroreceptor acts as a stretch receptor (Tobian 1960;Skinner et al 1964;Fray 1980). If it is assumed that the baroreceptor is localized in the afferent arteriole with the juxtaglomerular cells, a search should be made for a mechanism by which stretch of the arteriolar wall could influence renin release from the juxtaglomerular cells.…”

Communications

“…The responses were reversed when the blood volume was reduced by exsanguination at a rate of 15 ml./min. There is good evidence to suggest that renal arterial pressure is one factor controlling renin secretion (Tobian, 1960;Skinner, McCubbin & Page, 59P 10PPROCEEDINGS OF THE 1964). In our experiments the increases in blood volume caused little or no change in arterial pressure but proportionately large changes in central venous pressure.…”