Greater Antihypertensive Efficacy of the Calcium Channel Inhibitor Verapamil in Older and Low Renin Patients

1982 ◽  
Vol 63 (s8) ◽  
pp. 439s-442s ◽  
Author(s):  
Fritz R. Bühler ◽  
U. Lennart Hulthén ◽  
Wolfgang Kiowski ◽  
Peter Bolli
Keyword(s):  
Blood Pressure ◽  
Diastolic Pressure ◽  
Calcium Influx ◽  
Plasma Renin ◽  
Antihypertensive Efficacy ◽  
Mean Blood Pressure ◽  
Noradrenaline Concentration ◽  
Slow Channel ◽  
Sympathetic Nervous ◽  
Antihypertensive Response

1. The calcium slow channel inhibitor verapamil was administered as monotherapy (240-270 mg; mean 427 mg/day) on the average for 93 days to 43 patients with essential hypertension; 11 with low, 24 with normal and eight with high renin sodium index. 2. Verapamil reduced blood pressure from 171 ± 16/108 ± sd 6 mmHg to 152 ± 14/93 ± 9 (both P < 0.001); in 25 of the 43 patients a diastolic pressure ≤95 mmHg was achieved. Two patients each reported vertigo, sleeplessness and constipation. 3. The fall in mean blood pressure after verapamil was directly related to age (r = 0.759, P < 0.001), pretreatment mean blood pressure (r = 0.701, P < 0.01) and plasma noradrenaline concentration (r = 0.400, P < 0.05), and inversely related to plasma renin activity (r = −0.551), P < 0.001). These correlations were also significant for diastolic blood pressure. Accordingly, the antihypertensive response to verapamil was greatest in older and low renin patients. 4. This greater blood pressure decrease with verapamil in older and low renin patients suggests a greater calcium influx-dependent vasoconstriction in these patients, which seems to be directly related to the activity of the sympathetic nervous system.

Effect of alcohol withdrawal on blood pressure, plasma renin activity, aldosterone, cortisol and dopamine β-hydroxylase

1984 ◽  
Vol 66 (6) ◽  
pp. 659-663 ◽  
Author(s):  
L. T. Bannan ◽  
J. F. Potter ◽  
D. G. Beevers ◽  
J. B. Saunders ◽  
J. R. F. Walters ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Alcohol Withdrawal ◽  
Diastolic Pressure ◽  
Urine Volume ◽  
Plasma Renin ◽  
Renin Activity ◽  
Withdrawal Symptoms ◽  
Urinary Volume ◽  
Blood Pressures

1. Sixty-five alcoholic patients admitted for detoxification had blood pressure, withdrawal symptoms, plasma cortisol (PC) and plasma aldosteron (PA) levels, plasma renin activity (PRA), and serum dopamin β-hydroxylase (DBH) levels measured on the first and fourth days after admission. 2. On the morning after admission blood pressure was elevated (>140/90) in 32 patients (49%) and was 160/95mmHg or more in 21 (32%). PRA was initially elevated in 41 patients, PA levels in 14, and 13 patients had raised PC levels. By the fourth day, blood pressure and bio-chemical measures had fallen significantly while urine volume and sodium output, low on admission, had increased significantly. On admission urinary metanephrine levels were raised in four out of the 31 patients who had them measured. 3. The height of both the systolic and diastolic blood pressures was significantly related to the severity of the alcohol. withdrawal symptoms. Of the biochemical parameters measured, PC level correlated with systolic but not diastolic pressure, and urinary volume was inversely correlated with the height of the diastolic pressure. No relationship was found between blood pressure and PRA or PA level. 4. The pressor effect of alcohol withdrawal could be due to sympathetic nervous system overactivity, or possibly to hypercortisolaemia. The first hypothesis seems more likely.

Hormonal responses to synthetic atrial natriuretic peptide in patients on regular hemodialysis

1988 ◽  
Vol 119 (2) ◽  
pp. 257-262 ◽  
Author(s):  
Sadao Nakajima ◽  
Hiromichi Suzuki ◽  
Yo Kageyama ◽  
Takashi Takita ◽  
Takao Saruta
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Arterial Blood ◽  
Sympathetic Nervous ◽  
Regular Hemodialysis

Abstract. The effects of atrial natriuretic peptide (ANP) on mean arterial blood pressure, heart rate, plasma renin activity, aldosterone, cortisol, norepinephrine, epinephrine and arginine vasopressin were studied in 6 anuric subjects receiving regular hemodialysis. An iv bolus injection of 8 nmol of ANP followed by infusion at 32 pmol·kg−1·min−1 for 1 h in the pre- and posthemodialysis period was performed. Basal plasma ANP was higher before than after hemodialysis. ANP administration produced a reduction in mean arterial blood pressure accompanied by an elevation of norepinephrine and of plasma renin activity (from 2.49 ± 0.52 to 3.39 ± 0.85 nmol·l−1·h−1 predialysis and from 2.78 ± 0.71 to 3.15 ± 0.86 nmol·l−1·h−1 postdialysis, respectively, mean ± sem; P < 0.05). Plasma aldosterone and cortisol were significantly decreased. Plasma epinephrine and AVP remained unchanged. These hemodynamic and hormonal changes were similar in the pre- and the postdialysis period. These results suggest that 1) ANP causes a fall in mean arterial blood pressure, which in turn induces reflex tachycardia and activation of the sympathetic nervous system without diuresis; 2) the activated sympathetic nervous system as reflected in elevation of plasma norepinephrine may increase plasma renin activity; 3) reduced plasma aldosterone is not influenced by enhancement of the reninangiotensin system; therefore, 4) reduction of plasma aldosterone as well as cortisol is probably due to direct action of ANP, and finally 5) AVP had no direct relation with ANP administration.

Acute effect of labetalol on blood pressure in relation to the sympathetic nervous system and plasma renin activity

1984 ◽  
Vol 35 (6) ◽  
pp. 782-787 ◽  
Author(s):  
Nicolas D Vlachakis ◽  
John Barr ◽  
Manuel Velasquez ◽  
Natalie Alexander ◽  
Robert Maronde
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Acute Effect ◽  
Renin Activity ◽  
Sympathetic Nervous

Acute effects of moderate alcohol consumption on blood pressure and plasma catecholamines

1984 ◽  
Vol 66 (6) ◽  
pp. 643-647 ◽  
Author(s):  
M. A. Ireland ◽  
R. Vandongen ◽  
L. Davidson ◽  
L. J. Beilin ◽  
I. L. Rouse
Keyword(s):  
Blood Pressure ◽  
Drinking Water ◽  
Alcohol Consumption ◽  
Systolic Blood Pressure ◽  
Diastolic Pressure ◽  
Plasma Catecholamines ◽  
Acute Effects ◽  
Drinking Alcohol ◽  
Plasma Adrenaline ◽  
Noradrenaline Concentration

1. This study examines the response of blood pressure, plasma catecholamines and cortisol to acute alcohol intake in young men with light to moderate drinking habits. 2. Ingestion of alcohol was associated with a highly significant increase in systolic blood pressure and heart rate which occurred before blood alcohol reached its peak concentration of 16.9 ± 1.1 mmol/l (80 mg/100 ml). After an initial non-specific rise, diastolic pressure fell below values observed after drinking water only. This predominant effect of alcohol on systolic blood pressure is also seen with chronic alcohol consumption. 3. Drinking water and non-alcoholic cold liquids caused a marked fall in plasma adrenaline and a transient rise in noradrenaline concentration. In contrast, drinking alcohol resulted in a relative rise in adrenaline and a delayed increase in noradrenaline concentration. 4. Blood glucose increased after alcohol, supporting a physiological effect of adrenaline on liver glycogenolysis. Plasma cortisol concentration was also significantly higher after drinking alcohol. 5. It is proposed that the relative rise in adrenaline together with higher cortisol levels, repeated over a variable period in susceptible individuals, are implicated in the elevation of blood pressure associated with long term alcohol consumption. It concurs with observations in man and experimental animals of a slow pressor mechanism mediated by adrenaline. 6. The study emphasized that an evaluation of the acute effects of alcohol requires careful measurement of blood pressure, precise assay of catecholamines and recognition of the confounding effects of drinking cold liquids.

Angiotensin II Blockade before and after Marked Sodium Depletion in Patients with Hypertension

1978 ◽  
Vol 54 (1) ◽  
pp. 75-83 ◽  
Author(s):  
P. Van Hoogdalem ◽  
A. J. M. Donker ◽  
F. H. H. Leenen
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Hypotensive Effect ◽  
Renin Activity ◽  
Mean Blood Pressure ◽  
Sodium Depletion ◽  
Before And After

1. Angiotensin II blockade before and after marked sodium depletion in patients with hypertension [unilateral renovascular (eight), bilateral renovascular (four) and essential (four)] was performed by intravenous administration of the angiotensin II antagonist Sar1-Ala8-angiotensin II (saralasin). 2. On normal sodium intake, saralasin decreased mean blood pressure by 8 mmHg in the unilateral renovascular group, by 6 mmHg in the bilateral renovascular group and increased it by 3 mmHg in the essential hypertensive group. After sodium depletion saralasin decreased mean blood pressure by 33 mmHg, 35 mmHg and 18 mmHg respectively. The saralasin-induced decrease in blood pressure significantly correlated with the log of the initial plasma renin activity. 3. Saralasin infusion decreased effective renal plasma flow (ERPF) in all three hypertension subgroups, both on normal sodium intake and after sodium depletion. Glomerular filtration rate decreased in direct relation to the hypotensive effect of saralasin but ERPF showed this relationship only after sodium depletion. On normal sodium intake saralasin increased filtration fraction by 17%, but decreased it by 7% after sodium depletion. 4. It is concluded that the hypotensive action of saralasin closely correlates with the value of circulating plasma renin activity, apparently independent of the aetiology of the hypertension. The decrease in ERPF during saralasin infusion in the patients on normal sodium intake seems mainly related to the agonistic activity of saralasin, but that after sodium depletion to the hypotensive effect of saralasin.

scholarly journals Altered Neural and Vascular Mechanisms in Hypertension

2011 ◽  
pp. 381-402 ◽  
Author(s):  
M. PINTÉROVÁ ◽  
J. KUNEŠ ◽  
J. ZICHA
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
G Proteins ◽  
High Blood Pressure ◽  
Calcium Current ◽  
Calcium Influx ◽  
Dominant Role ◽  
Cardiovascular Complications ◽  
Sympathetic Nervous

Essential hypertension is a multifactorial disorder which belongs to the main risk factors responsible for renal and cardiovascular complications. This review is focused on the experimental research of neural and vascular mechanisms involved in the high blood pressure control. The attention is paid to the abnormalities in the regulation of sympathetic nervous system activity and adrenoceptor alterations as well as the changes of membrane and intracellular processes in the vascular smooth muscle cells of spontaneously hypertensive rats. These abnormalities lead to increased vascular tone arising from altered regulation of calcium influx through L-VDCC channels, which has a crucial role for excitation-contraction coupling, as well as for so-called “calcium sensitization” mediated by the RhoA/Rho-kinase pathway. Regulation of both pathways is dependent on the complex interplay of various vasodilator and vasoconstrictor stimuli. Two major antagonistic players in the regulation of blood pressure, i.e. sympathetic nervous system (by stimulation of adrenoceptors coupled to stimulatory and inhibitory G proteins) and nitric oxide (by cGMP signaling pathway), elicit their actions via the control of calcium influx through L-VDCC. However, L-type calcium current can also be regulated by the changes in membrane potential elicited by the activation of potassium channels, the impaired function of which was detected in hypertensive animals. The dominant role of enhanced calcium influx in the pathogenesis of high blood pressure of genetically hypertensive animals is confirmed not only by therapeutic efficacy of calcium antagonists but especially by the absence of hypertension in animals in which L-type calcium current was diminished by pertussis toxin-induced inactivation of inhibitory G proteins. Although there is considerable information on the complex neural and vascular alterations in rats with established hypertension, the detailed description of their appearance during the induction of hypertension is still missing.

Influence of the sympathetic nervous system and vasopressin on the blood pressure lowering effect of nifedipine in deoxycorticosterone acetate–salt hypertensive rats

1987 ◽  
Vol 73 (3) ◽  
pp. 253-258 ◽  
Author(s):  
Yutaka Takata ◽  
Yoshiaki Yamashita ◽  
Shuichi Takishita ◽  
Masatoshi Fujishima
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Calcium Influx ◽  
Hypotensive Effect ◽  
Ang Ii ◽  
Hypertensive Rats ◽  
Blood Pressure Lowering Effect ◽  
Hypotensive Action ◽  
Sympathetic Nervous

1. The role of the sympathetic nervous system and the effect of vasopressin (AVP) on the hypotensive action of nifedipine (Nf) were evaluated in conscious, unrestrained normotensive and DOCA–salt hypertensive rats. 2. The hypotensive response to Nf was much greater in DOCA rats than in the controls. 3. Solitary blockade of the sympathetic nervous system or AVP, did not alter the Nf effect in either DOCA or control rats. However, a combination clearly diminished the effect of Nf in the DOCA group, but enhanced it in the controls. The inhibition of angiotensin II (ANG II) augmented the hypotensive effect of Nf in control animals, but not in the DOCA rats. The percentage fall in blood pressure with Nf was much the same in both groups after the combined inhibition of the sympathetic nervous system and AVP. 4. The enhanced hypotensive action of Nf in DOCA rats may be dependent on the hyperactivity of the sympathetic nervous system and AVP, which facilitates calcium influx, and in the normotensive animals the depressor response to Nf may relate to blockade of the calcium influx, independent of the sympathetic nervous system, AVP and ANG II.

Pre-operative evaluation of the prognosis of hypertension in primary aldosteronism owing to adenoma

1987 ◽  
Vol 116 (2) ◽  
pp. 229-234 ◽  
Author(s):  
Takao Saruta ◽  
Hiromichi Suzuki ◽  
Takashi Takita ◽  
Ikuo Saito ◽  
Masaru Murai ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Primary Aldosteronism ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
The Other ◽  
Mean Blood Pressure ◽  
Plasma Aldosterone Concentration ◽  
Postoperative Prognosis ◽  
History Of ◽  
Family History Of Hypertension

Abstract. The prognosis of hypertension was evaluated pre-operatively in 40 patients with primary aldosteronism owing to adenoma by examining the severity of hypertension, family history of hypertension, age of the patients, duration of hypertension, plasma renin activity, plasma aldosterone concentration, and efficacy of spironolactone (100 mg per day for 10 days) on blood pressure. In 30 of the 40 patients, the blood pressure was reduced to below 160/95 mmHg within a year after adrenalectomy (responders). In the other 10 patients, the blood pressure was not markedly reduced and remained above 160/95 mmHg (nonresponders). There were no significant differences in the age of the patients, family history of hypertension, plasma renin activity or plasma aldosterone concentration between these two groups. The severity of hypertension as judged by the WHO classification and the duration of hypertension prior to operation seemed to be of some use in assessing the postoperative prognosis of hypertension, but the efficacy of spironolactone was far more useful. That is to say, a reduction in mean blood pressure of more than 15 mmHg after administration of spironolactone was observed in 29 of the 30 responders. The remaining one patient showed an 11 mmHg reduction in mean blood pressure. On the other hand, none of the nonresponders revealed a reduction in mean blood pressure of more than 15 mmHg after spironolactone administration. From these results it is concluded that the pre-operative response of blood pressure to administration of 100 mg per day of spironolactone for 10 days represents a useful indicator of the postoperative prognosis of hypertension in patients with primary aldosteronism owing to adenoma.

AT1 and TxA2/PGH2 receptors maintain hypertension throughout 2K,1C Goldblatt hypertension in the rat

1996 ◽  
Vol 271 (4) ◽  
pp. R891-R896 ◽  
Author(s):  
C. S. Wilcox ◽  
J. Cardozo ◽  
W. J. Welch
Keyword(s):  
Blood Pressure ◽  
Receptor Antagonist ◽  
Sodium Intake ◽  
Late Phase ◽  
Plasma Renin ◽  
Type I ◽  
Ang Ii ◽  
Control Groups ◽  
The Mean ◽  
Antihypertensive Response

Angiotension II (ANG II) increases the generation of vasoconstrictor prostaglandin endoperoxides (PGH2) and thromboxane A2 (TxA2). Two-kidney, one-clip (2K,1C) Goldblatt hypertensive rats have an increased plasma renin activity (PRA) and ANG II level during the early, but not the late, phases of hypertension. Therefore, the aim of these studies was to compare the antihypertensive efficacy of an ANG II type I (AT1) and a TxA2/PGH2 receptor antagonist during different phases of 2K,1C hypertension. Rats were maintained on a fixed sodium intake for 3 days before and throughout the period of drug administration. These studies assessed the antihypertensive response to administration of the AT1 receptor antagonist losartan (20 mg.kg-1.day-1), the TxA2/PGH2 receptor antagonist ifetroban (20 mg.kg-1.day-1) or vehicle given for 3 days to rats with early (2-4 wk postclip), intermediate (10-12 wk postclip), and late (36-42 wk post-clip) 2K,1C hypertension and to two control groups of rats corresponding in age to the early or intermediate and the late 2K,1C groups. The mean arterial pressure (MAP) was measured directly with indwelling arterial cannulas. The MAP of sham-operated rats was 109 +/- 5 mmHg. In the early phase of 2K,1C hypertension, the MAP was increased to 143 +/- 6 mmHg, and it was increased further to 162 +/- 5 mmHg during the intermediate and to 179 +/- 4 mmHg during the late phase. The PRA, compared with age-matched controls, was increased during early and intermediate, but not late phase 2K,1C hypertension. Neither drug lowered blood pressure in control rats. However, both drugs significantly reduced the blood pressure in the early, intermediate, and late phases of 2K, 1C hypertension. At the end of 3 days of administration, blood pressure in early 2K, 1C rats given losartan was reduced to levels of control rats, but remained slightly elevated in other groups and in those receiving ifetroban. In conclusion, AT1 and TxA2/PGH2 receptors maintain hypertension throughout the evolution of 2K, 1C hypertension in the rat, despite changes in PRA.

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