The role of the kidney in essential hypertension

Abstract

1. Many forms of human and experimental hypertension begin with compromised renal function. Essential hypertension may be another such case. 2. The kidneys of subjects with essential hypertension excrete normal amounts of salt and water at higher-than-normal renal perfusing pressures. Other overt signs of renal dysfunction are few; renal disease is excluded by definition. However, renal blood flow and glomerular filtration rate are usually less than normal in essential hypertension. 3. Renal afferent resistance can be calculated from arterial pressure, renal blood flow, and an estimate of glomerular capillary pressure. These calculations indicate that afferent resistance is increased to two or more times normal in essential hypertension. 4. It is not clear whether afferent constriction causes hypertension or results from it. The ability of high pressure to produce vascular damage points to the latter. But, most essential hypertensives show low-to-normal plasma renin levels and a marked afferent dilation after saline loading. These observations do not suggest nephrosclerosis: they are consistent with a causal role for afferent constriction. 5. We can speculate that, in essential hypertension, there is a defect in one of the mechanisms that sets afferent resistance. Afferent constriction could result from extrinsic influences (neural or humoral) or something totally within the kidney, such as abnormal handling of information from the macula densa. 6. The effect of afferent constriction on salt-and-water excretion would theoretically be offset by elevated arterial pressure so that the actual salt-and-water excretion would be normal, but only so long as the arterial pressure remained elevated.

The antihypertensive mechanism of verapamil. Alteration of glomerular filtration rate regulation.

“…However, one of the hallmarks of essential hypertension is greatly elevated renal vascular resistance. 20 We observed a significant stimulatory effect of verapamil on the renin release rate that was most clearly apparent at reduced perfusion pressure levels. At the 100 and 90 mm Hg levels the release rates of the two groups were not significantly different (see Table 1); however, the difference became progressively greater as perfusion pressure was lowered.…”

Sympathetic vascular tone in spontaneous hypertension of rats

“…This may be explained in part by theoretical considerations since the volume concept of hypertension [3,11] has concentrated most of the research work in the field of hypertension on renal and volume factors during the past decade. On the other hand, there are methodological problems in evaluation of sympathetic activity and its effect on the target organs.…”

“…The volume concept of hypertension [3,11] postulates a primary increase in plasma volume as a consequence of a diminished sodium fluid excreting capability of the kidneys. This concept denies the possibility of a primary increase in peripheral resistance as the cause of high blood pressure, since any deviation of blood pressure would be corrected by the kidney with infinite feedback gain [3,11].…”

Abnormal pressure natriuresis. A cause or a consequence of hypertension?

“…Initially, the hypertension is caused by impaired function of the clipped kidney, while the contralateral intact kidney undergoes natriuresis, which partly ameliorates the hypertension. 41 Full compensation for impaired function of the clipped kidney is not achieved by the contralateral kidney because its excretory function is also partly attenu-ated by various functional changes, such as increased circulating Ang II.…”

“…For example, renal vascular resistance is almost invariably increased in patients with essential hypertension. 41 -6869 Yet, high renal vascular resistance could be an autoregulatory response to increased blood pressure in some cases or it could play a causal role in others if it is increased sufficiently to lower renal blood flow and GFR.…”