Salt and hypertension: water-sodium handling in essential hypertension.
This paper describes sodium handling in the kidney and the significance and mechanisms of its effects upon essential hypertension. In patients with low renin essential hypertension, plasma and urinary norepinephrine levels, plasma renin activity and fractional excretion of sodium were significantly lower, while plasma volume, extracellular fluid volume and exchangeable sodium were higher than in normal renin essential hypertension. The suppression of some renal depressor-natriuretic systems, the dopaminergic, kallikrein-kinin and prostaglandin E2 systems may contribute to the retention of sodium-water in these patients, because these depressor systems were observed to be greatly suppressed in essential hypertension, especially in the low renin group. The reduction of conversion from L-dopa to dopamine by dopa-decarboxylase in the proximal tubules was suggested from our clearance studies as the mechanism of the suppression of renal dopaminergic activity. Moreover, renal dopaminergic activity was already suppressed at the prehypertensive stage, possibly through the inhibition of renal dopa-decarboxylase activity. Thus, it appears that the suppression of renal depressor-natriuretic systems play an important role in the pathogenesis of essential hypertension through the retention of sodium and body fluid volume.
Iimura
O
O
Second Department of Internal Medicine, Sapporo Medical College, Japan.
Shimamoto
K
K
D001834:Body Water / Q000378:metabolism*; D004298:Dopamine / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D007610:Kallikreins / Q000502:physiology; D007668:Kidney / Q000503:physiopathology; D011458:Prostaglandins E / Q000502:physiology; D012083:Renin / Q000097:blood; D012964:Sodium / Q000378:metabolism*
D011458:Prostaglandins E; D012964:Sodium; D007610:Kallikreins; D012083:Renin; D004298:Dopamine