Multiple oral doses of nicardipine, a calcium-entry blocker: Effects on renal function, plasma renin activity, and aldosterone concentration in mild-to-moderate essential hypertension

1. Stepwise increases of oral doses of propranolol produced both a significant lowering of blood pressure and suppression of plasma renin activity in sixteen patients with mild or moderate normal-renin essential hypertension. 2. The hypotensive and the renin-suppressive actions of propranolol were differently related to plasma propranolol concentrations. At the lowest propranolol concentrations (15–40 nmol/l), there was almost no decrease in blood pressure whereas plasma renin activity and responsiveness to renin-releasing stimuli (standing, intravenous frusemide) were already strongly depressed (greater than 50%). Therefore in a large number of normal-renin hypertensive patients under small doses of propranolol, the renin-suppressive action of the drug can be dissociated from the hypotensive effect. Dissociation of the two effects, though in the opposite way, was also observed in three of four low-renin hypertensive patients, whose blood pressure was decreased by propranolol without further reduction of the already suppressed plasma renin activity. 3. It is concluded that in patients with mild and moderate hypertension and low or normal plasma renin activity, the hypotensive effect of propranolol cannot be attributed to suppression of renin activity. These conclusions do not necessarily apply to high-renin hypertensive patients.

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Plasma renin activity in the diagnosis of primary aldosteronism: failure to distinguish primary aldosteronism from essential hypertension

Archives of Internal Medicine ◽

10.1001/archinte.123.2.141 ◽

1969 ◽

Vol 123 (2) ◽

pp. 141-146 ◽

Cited By ~ 10

Author(s):

A. Jose

Keyword(s):

Essential Hypertension ◽

Plasma Renin Activity ◽

Primary Aldosteronism ◽

Plasma Renin ◽

Renin Activity

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125 Increased plasma renin activity during wake in a repetitive sleep restriction protocol

SLEEP ◽

10.1093/sleep/zsab072.124 ◽

2021 ◽

Vol 44 (Supplement_2) ◽

pp. A51-A51

Author(s):

Huan Yang ◽

Michael Vazquez ◽

Monika Haack ◽

Janet Mullington

Keyword(s):

Renal Function ◽

Plasma Renin Activity ◽

Impaired Renal Function ◽

Plasma Renin ◽

Renin Activity ◽

Sleep Restriction ◽

Science Center ◽

Percent Change ◽

Recovery Sleep ◽

Increased Risk

Abstract Introduction Insufficient sleep is associated with an increased risk of hypertension. It is well established that long-term BP regulation is modulated by the renin-angiotensin-aldosterone system (RAAS) and chronic kidney disease is a strong independent risk factor for development of cardiovascular disease. This study investigated the biomarkers of RAAS and renal function during repetitive exposures to controlled, experimental sleep restriction (SR). We hypothesized an upregulation of RAAS and increased markers of impaired renal function. Methods Twenty-one healthy participants (11 women, average age 31±2 years) completed the 22-day in-hospital SR protocol: permitted 4h of sleep/night from 0300-0700 for 3 nights followed by a recovery sleep, repeated 4 times. Blood samples were collected and plasma renin activity (PRA) was assessed in the morning (7:05am) and in the evening before bedtime (22:45pm) at baseline, experimental days (3rd day of each of the 4 blocks), and recovery. Urinary albumin to creatinine ratio (ACR) was measured from 24-h urinary collection at baseline, first and fourth SR blocks. Estimated glomerulus filtration rate (eGFR) was calculated based on the serum cystatin C levels at baseline and last block of SR. Results Percent change of evening PRA significantly increased during 4 blocks of SR and recovery (SR effect p=0.039), but not morning PRA (SR effect p=0.34). Specifically, evening PRA increased up to 98.4% in the first (p<0.01), 61.3% in the second (p=0.04) SR blocks, and 57.5% (p=0.05) in recovery. Urinary ACR showed no significant changes during first or fourth SR blocks (SR effect p=0.28). In addition, eGFR did not change in the fourth SR block compared to BL (paired t-test, p=0.27). Conclusion We did not see increased markers of impaired renal function (ACR or eGFR). Rather, short-term repetitive exposures to SR significantly increased percent change of PRA measured before bedtime, and evening PRA did not return to BL level during recovery. Our results suggested that sleep deficiency may contribute to hypertension through upregulation of RAAS during wake time. Support (if any) SRSF (CDA to Huan Yang), NIH (R01HL106782 to Dr. Janet Mullington), Harvard Catalyst, Harvard Clinical and Translational Science Center (UL1TR001102).

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Dependence of plasma renin activity on prostaglandin excretion in essential hypertension

Acta Physiologica Scandinavica ◽

10.1111/j.1748-1716.1978.tb06052.x ◽

1978 ◽

Vol 102 (1) ◽

pp. 120-122 ◽

Cited By ~ 5

Author(s):

Pauli Yuitalo ◽

Heikki Vapaatalo ◽

Timo Metsä-Ketelä ◽

Timo Pitkäjärvi

Keyword(s):

Essential Hypertension ◽

Plasma Renin Activity ◽

Plasma Renin ◽

Renin Activity

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Diuretics in hypertension

Drug and Therapeutics Bulletin ◽

10.1136/dtb.13.26.101 ◽

1975 ◽

Vol 13 (26) ◽

pp. 101-103

Keyword(s):

Essential Hypertension ◽

Plasma Renin Activity ◽

Thiazide Diuretic ◽

Mild Hypertension ◽

Antihypertensive Drugs ◽

Antihypertensive Agents ◽

Plasma Renin ◽

Renin Activity ◽

Thiazide Diuretics ◽

Treatment Of Hypertension

Thiazide diuretics such as bendrofluazide and chlorothiazide have been used for nearly 20 years in the treatment of hypertension. They have been regarded as rather weak antihypertensive agents which could be used alone only in mild hypertension and otherwise as adjuvants to more potent drugs in more serious cases.1 There are however some patients with ‘essential’ hypertension who are very sensitive to diuretics and in whom the pressure may be brought down to normal by a thiazide2 or spironolactone3 even when it is initially considerably raised. Furthermore a few patients who are responsive to thiazides are strikingly unresponsive to non-diuretic antihypertensive drugs. Patients particularly likely to respond to a thiazide diuretic4 or spironolactone3 commonly have low plasma renin activity and this occurs in about 25% of patients with essential hypertension.5 Since plasma renin activity is not routinely estimated it is simplest to identify these patients by observing the response to an adequate trial of a thiazide.

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Solitary Kidney and Ageing as Causes of Low Renin and Aldosterone Concentrations: Relevance to ‘Low-Renin’ Essential Hypertension

Clinical Science ◽

10.1042/cs051177s ◽

1976 ◽

Vol 51 (s3) ◽

pp. 177s-180s ◽

Cited By ~ 1

Author(s):

R. Gordon ◽

Freda Doran ◽

M. Thomas ◽

Frances Thomas ◽

P. Cheras

Keyword(s):

Blood Pressure ◽

Essential Hypertension ◽

Plasma Renin Activity ◽

Plasma Volume ◽

Plasma Renin ◽

Renin Activity ◽

Dietary Sodium ◽

Sodium Restriction ◽

Normotensive Subjects ◽

The Mean

1. As experimental models of reduced nephron population in man, (a) twelve men aged 15–32 years who had one kidney removed 1–13 years previously and (b) fourteen normotensive men aged 70–90 years were studied. Results were compared with those in eighteen normotensive men aged 18–28 years and eleven men aged 19–33 years with essential hypertension. 2. While the subjects followed a routine of normal diet and daily activity, measurements were made, after overnight recumbency and in the fasting state, of plasma volume and renin activity on one occasion in hospital and of blood pressure on five to fourteen occasions in the home. Blood pressure was also measured after standing for 2 min and plasma renin activity after 1 h standing, sitting or walking. Twenty-four hour urinary aldosterone excretion was also measured. 3. The measurements were repeated in the normotensive subjects and subjects in (a) and (b) above after 10 days of sodium-restricted diet (40 mmol of sodium/day). 4. The mean plasma renin activity (recumbent) in essential hypertensive subjects was higher than in normotensive subjects. In subjects of (a) and (b) above, it was lower than normotensive subjects, and was not increased by dietary sodium restriction in subjects of (a). 5. The mean aldosterone excretion level was lower in old normotensive subjects than in the other groups, and increased in each group after dietary sodium restriction. 6. Mean plasma volume/surface area was not different between the four groups and in normotensive, essential hypertensive and nephrectomized subjects but not subjects aged 70–90 years was negatively correlated with standing diastolic blood pressure.

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