The effect of 8 weeks treatment with the calcium antagonist felodipine on blood pressure, heart rate, working capacity, plasma renin activity, plasma angiotensin II, urinary catecholamines and aldosterone in patients with essential hypertension.

1. The renin-angiotensin and kinin-kallikrein systems of Dahl salt-sensitive and salt-resistant rats fed diets with different salt contents were analysed using biochemical and immunocytochemical techniques. 2. Blood pressure increased by 45% in salt-sensitive rats only, after 4 weeks on a high-salt diet. The plasma renin activity and plasma angiotensin II concentration remained at the same levels in salt-sensitive rats on the high-salt diet as on the normal salt diet, whereas the plasma renin activity and plasma angiotensin II concentration of salt-resistant rats fed the high-salt diet were lower. The plasma renin activity and the plasma angiotensin II concentration were elevated in both salt-resistant and salt-sensitive rats fed the salt-deficient diet but were much more elevated in salt-resistant than in salt-sensitive rats. 3. The kidney immunocytochemical data paralleled the data on plasma parameters. Salt-sensitive rats had fewer renin positive juxtaglomerular apparatuses than salt-resistant rats on the normal diet, and the increase on the sodium-deficient diet was also smaller in salt-sensitive rats. Salt-sensitive rats fed the high-salt diet and the standard diet had almost no angiotensin II immunoreactivity compared with the salt-resistant rats on the same diets. 4. The total renal kallikrein content of salt-sensitive rats was lower than that of salt-resistant rats on all three diets, as was the amount of kallikrein excreted in the urine on the standard and the high-salt diets. The differences resulted from a reduction in active kallikrein. The increase in kallikrein in salt-sensitive and salt-resistant rats on the salt-deficient diet was not significantly different. 5. There were similar changes in immunopositive kallikrein in the kidneys of salt-sensitive and salt-resistant rats with diet, with a large increase in kallikrein biosynthesis on the low-salt diet. The plasma concentration of high-molecular-mass kininogen was not significantly different in salt-sensitive and salt-resistant rats, but there was a significant increase in T-kininogen in salt-sensitive rats fed the high-salt diet. 6. In conclusion, the absence of decreases in the plasma renin activity and the plasma angiotensin II concentration in salt-sensitive rats fed the high-salt diet might partially explain the increase in blood pressure.

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Effects of opioid antagonism on the haemodynamic and hormonal responses to exercise

Clinical Science ◽

10.1042/cs0750293 ◽

1988 ◽

Vol 75 (3) ◽

pp. 293-300 ◽

Cited By ~ 10

Author(s):

Jan Staessen ◽

Roberto Fiocchi ◽

Roger Bouillon ◽

Robert Fagard ◽

Peter Hespel ◽

...

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Angiotensin Ii ◽

Plasma Renin Activity ◽

Serum Insulin ◽

Plasma Renin ◽

Endogenous Opioids ◽

Renin Activity ◽

Plasma Adrenaline ◽

Noradrenaline And Adrenaline

1. Physical effort involves, along with an increase in the plasma concentration of β-endorphin, profound adaptations of the circulation and the endocrine system. The effects of opioid antagonism on the responses of blood pressure, heart rate and several hormones to exercise were therefore studied in 10 normal men. They exercised in the supine position up to 33% and 66% of their maximal exercise capacity and received in a randomized double-blind cross-over protocol, either saline or naloxone (10 mg intravenously, followed by a continuous infusion of 10 mg/h). 2. Intra-arterial pressure and heart rate were continuously monitored, but were not affected by naloxone. 3. At rest, opioid antagonism produced a rise in plasma renin activity and in plasma adrenocorticotropin, Cortisol and aldosterone, but only the stimulation of the two adrenocortical hormones differed significantly from the control experiments; at rest naloxone also prevented the fall in plasma adrenaline, which occurred with saline infusion. Furthermore, the exercise-induced rises in plasma angiotensin II, aldosterone, Cortisol, noradrenaline and adrenaline were higher on naloxone than on saline, while a similar tendency was also present for the increases with exercise in plasma renin activity and plasma adrenocorticotropin. Neither at rest nor during exercise did opioid antagonism alter plasma lactate and glucose and serum insulin and growth hormone. 4. In conclusion, (1) endogenous opioids are not involved in the responses of blood pressure and heart rate to supine exercise; (2) at rest and during exercise, the endogenous opioids inhibit the secretion of adrenocorticotropin, aldosterone, Cortisol, noradrenaline and adrenaline; (3) they also inhibit the plasma renin-angiotensin II system indirectly via the catecholamines.

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Plasma renin activity, angiotensin II, and aldosterone during intense heat stress

Journal of Applied Physiology ◽

10.1152/jappl.1976.41.3.323 ◽

1976 ◽

Vol 41 (3) ◽

pp. 323-327 ◽

Cited By ~ 52

Author(s):

K. J. Kosunen ◽

A. J. Pakarinen ◽

K. Kuoppasalmi ◽

H. Adlercreutz

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Heat Stress ◽

Angiotensin Ii ◽

Plasma Renin Activity ◽

Plasma Renin ◽

Renin Activity ◽

Arterial Blood ◽

Main Components ◽

Intense Heat

Plasma renin activity (PRA), angiotensin II, and aldosterone levels, arterial blood pressure, and heart rate of six male students were investigated during and after heat stress in a sauna bath. Increased PRA, angiotensin II, and aldosterone levels were found both during and after sauna. The greatest mean increases in PRA (94.9 +/- 10.4% SE, P less than 0.005) and angiotensin II (196 +/- 54.7% SE, P less than 0.02) were observed at the end of the heat stress (at 20 min), and that in plasma aldosterone (505 +/- 209% SE, P less than 0.02) 30 min after the sauna. The heart rate roughly doubled during the heat stress and there was a transient increase followed by a decrease in systolic blood pressure and a decrease in diastolic blood pressure. This study demonstrates that intense heat stress can cause remarkable changes in the three main components of the renin-angiotensin-aldosterone system.

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Interrelations among blood pressure, blood volume, plasma renin activity and urinary catecholamines in benign essential hypertension

The American Journal of Medicine ◽

10.1016/0002-9343(77)90332-1 ◽

1977 ◽

Vol 62 (2) ◽

pp. A80

Keyword(s):

Blood Pressure ◽

Essential Hypertension ◽

Plasma Renin Activity ◽

Blood Volume ◽

Plasma Renin ◽

Renin Activity ◽

Urinary Catecholamines

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Interrelations among blood pressure, blood volume, plasma renin activity and urinary catecholamines in benign essential hypertension

The American Journal of Medicine ◽

10.1016/0002-9343(77)90316-3 ◽

1977 ◽

Vol 62 (2) ◽

pp. 209-218 ◽

Cited By ~ 65

Author(s):

Peter Weidmann ◽

David Hirsch ◽

Carlo Beretta-Piccoli ◽

Francois C. Reubi ◽

Walter H. Ziegler

Keyword(s):

Blood Pressure ◽

Essential Hypertension ◽

Plasma Renin Activity ◽

Blood Volume ◽

Plasma Renin ◽

Renin Activity ◽

Urinary Catecholamines

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Humoral Effects of the Oral Converting-Enzyme Inhibitor Sq 14 225 in Hypertensive Patients in Supine and Tilted Position

Clinical Science ◽

10.1042/cs057149s ◽

1979 ◽

Vol 57 (s5) ◽

pp. 149s-152s ◽

Cited By ~ 6

Author(s):

A. Morganti ◽

T. G. Pickering ◽

J. Lopez-Ovejero ◽

J. H. Laragh

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Nervous System ◽

Angiotensin Ii ◽

Plasma Renin Activity ◽

Plasma Renin ◽

Renin Activity ◽

Converting Enzyme ◽

Hypertensive Patients ◽

Sympathetic Nervous

1. To evaluate the effects of converting-enzyme inhibition on the sympathetic nervous system, on renin and on the other known regulators of aldosterone secretion, we measured blood pressure, heart rate, plasma noradrenaline, adrenaline, renin activity, aldosterone, cortisol and serum potassium in 15 sodium-repleted hypertensive patients in supine position and during 30 min of 65° head-up tilt before and during treatment with SQ 14 225. 2. SQ 14 225 produced significant decreases in supine blood pressure and plasma aldosterone and significant increments in plasma renin activity and potassium; in contrast, heart rate, noradrenaline, adrenaline and cortisol were unchanged. 3. While in control tilt studies blood pressure was always maintained, during treatment three of 15 patients had vasovagal syncopes. In the remaining 12 blood pressure was maintained during tilt on SQ 14 225; however, while the tilt-induced responses in heart rate and adrenaline were as in control studies, the 30 min increments in noradrenaline were significantly higher. 4. Both before and during treatment the responses of plasma renin activity and aldosterone to tilt were parallel, and correlated with each other, and cortisol and potassium changed only slightly. 5. It is concluded that the SQ 14 225-induced fall in blood pressure occurs without a concomitant rise in sympathetic nervous activity; thus the increase in supine plasma renin activity, being a reflection of the interruption of the angiotensin feedback mechanism on renin release, indicates an effective suppression of angiotensin II formation. 6. During SQ 14 225 the persistence of aldosterone response to tilt and its relationship with renin activity suggest that the enzymatic blockade is over-ridden; however, in the presence of a reduced formation of angiotensin II a more pronounced response of the sympathetic nervous system is required to defend blood pressure against postural changes.

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Lack of effect of Naloxone in a Moderate dosage on the Exercise-Induced Increase in Blood Pressure, Heart Rate, Plasma Catecholamines, Plasma Renin Activity and Plasma Aldosterone in Healthy Males

Clinical Science ◽

10.1042/cs0680185 ◽

1985 ◽

Vol 68 (2) ◽

pp. 185-191 ◽

Cited By ~ 13

Author(s):

Margareta Bramnert ◽

Hökfelt Bernt

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Plasma Renin Activity ◽

Plasma Catecholamines ◽

Plasma Renin ◽

Plasma Aldosterone ◽

Renin Activity ◽

Working Capacity ◽

Exercise Induced ◽

Maximal Working Capacity

1. There is evidence that opioid peptides influence blood pressure and heart rate in animals and man. In the present investigation the effect of naloxone on the exercise-induced increase in blood pressure, heart rate, plasma catecholamines, plasma renin activity (PRA) and plasma aldosterone was investigated in nine healthy men. A submaximal work test was performed on two occasions. The test consisted of ergometer bicycling for 10 min on 50% of maximal working capacity immediately followed by 10 min on 80% of maximal working capacity. Ten minutes before exercise the subjects received in a randomized manner a bolus dose of naloxone (10 μg/kg) or a corresponding volume of saline followed by a slow infusion (15 ml/h) of naloxone (5 μ h−1 kg−1) or saline, respectively. 2. After exercise systolic blood pressure, heart rate, plasma catecholamines, PRA and plasma aldosterone increased during both saline and naloxone infusion. The changes were similar in both studies. 3. Accordingly, opiate receptors sensitive to naloxone in a moderate dosage seem not to be involved in the cardiovascular response and the increase in plasma catecholamines, PRA and plasma aldosterone induced by exercise.

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High-Renin Essential Hypertension: Adrenergic Cardiovascular Correlates

Clinical Science ◽

10.1042/cs051181s ◽

1976 ◽

Vol 51 (s3) ◽

pp. 181s-184s ◽

Cited By ~ 3

Author(s):

M. Esler ◽

S. Julius ◽

O. Randall ◽

V. Dequattro ◽

A. Zweifler

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Essential Hypertension ◽

Plasma Renin Activity ◽

Peripheral Resistance ◽

Plasma Renin ◽

Normal Subjects ◽

Renin Activity ◽

Elevated Plasma ◽

Sympathetic Nervous

1. Patients with mild essential hypertension and elevated plasma renin activity, when compared with normal subjects and hypertensive subjects with normal plasma renin, demonstrated features of sympathetic nervous cardiovascular excitation, accompanied by a raised plasma noradrenaline concentration. 2. An elevated heart rate at rest, shortened cardiac pre-ejection period, and greater heart rate reduction with acute β-adrenoreceptor blockade (intravenous propranolol) in high-renin essential hypertension were indicative of adrenergic cardiac excitation. An elevated total peripheral vascular resistance at rest and a greater fall in peripheral resistance with α-adrenoreceptor blockade (intravenous phentolamine) suggested the existence of a neurogenic increase in arteriolar resistance. 3. Blood pressure was normalized by ‘total’ autonomic blockade (atropine plus propranolol plus phentolamine) in the hypertensive subjects with elevated plasma renin activity. 4. These findings suggest that in mild high-renin essential hypertension increased adrenergic drive to the heart and resistance vessels exists. The elevation of blood pressure is sustained predominantly by neurogenic mechanisms. The high plasma renin activity is seen as an expression of sympathetic nervous system overactivity.

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Renin, Blood Volume and Response to Saralasin in Patients on Chronic Haemodialysis: Evidence against Volume- and Renin-‘Dependent’ Hypertension

Clinical Science ◽

10.1042/cs0540305 ◽

1978 ◽

Vol 54 (3) ◽

pp. 305-312

Author(s):

B. P. McGrath ◽

J. G. G. Ledingham

Keyword(s):

Blood Pressure ◽

Angiotensin Ii ◽

Plasma Renin Activity ◽

Blood Volume ◽

Plasma Renin ◽

Renin Activity ◽

Mean Blood Pressure ◽

Dietary Sodium ◽

Chronic Haemodialysis ◽

Plasma Angiotensin

1. No significant relationship was found between blood pressure and blood volume, sulphate space or plasma angiotensin II concentration in 59 non-nephrectomized haemodialysis patients, of whom 42 were hypertensive. Supine mean blood pressure was only weakly correlated with plasma renin activity and the correlation was not improved when blood pressure was related to expressions combining renin and volume. 2. Changes in supine mean blood pressure during saralasin infusion were related to pre-infusion plasma renin activity (P < 0·001) or plasma angiotensin II (P < 0·02) but also to blood volume (P < 0·001) or sulphate space (P < 0·001). A fall of more than 10% in mean blood pressure during saralasin infusion was observed in only 12 patients (one normotensive), in five of whom there was evidence of volume depletion. 3. Thirteen patients (nine hypertensive) were studied at two levels of dietary sodium: 100 mmol/day and < 20 mmol/day. Supine mean blood pressure in hypertensive patients was lower during the period of higher salt intake despite increased volumes. 4. Hypertension in haemodialysis patients cannot be adequately explained by abnormalities either in volume homeostasis and/or in the renin—angiotensin system.

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Effect of enalapril (MK-421), an orally active angiotensin I converting enzyme inhibitor, on blood pressure, active and inactive plasma renin, urinary prostaglandin E2, and kallikrein excretion in conscious rats

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y84-019 ◽

1984 ◽

Vol 62 (1) ◽

pp. 116-123 ◽

Cited By ~ 15

Author(s):

Ernesto L. Schiffrin ◽

Jolanta Gutkowska ◽

Gaétan Thibault ◽

Jacques Genest

Keyword(s):

Blood Pressure ◽

Angiotensin Ii ◽

Plasma Renin Activity ◽

Plasma Renin ◽

Ace Inhibition ◽

Renin Activity ◽

Prostaglandin E ◽

Converting Enzyme ◽

Angiotensin I ◽

Angiotensin I Converting Enzyme

The angiotensin I converting enzyme (ACE) inhibitor enalapril (MK-421), at a dose of 1 mg/kg or more by gavage twice daily, effectively inhibited the pressor response to angiotensin I for more than 12 h and less than 24 h. Plasma renin activity (PRA) did not change after 2 or 4 days of treatment at 1 mg/kg twice daily despite effective ACE inhibition, whereas it rose significantly at 10 mg/kg twice daily. Blood pressure fell significantly and heart rate increased in rats treated with 10 mg/kg of enalapril twice daily, a response which was abolished by concomitant angiotensin II infusion. However, infusion of angiotensin II did not prevent the rise in plasma renin. Enalapril treatment did not change urinary immunorcactive prostaglandin E2 (PGE2) excretion and indomethacin did not modify plasma renin activity of enalapril-treated rats. Propranolol significantly reduced the rise in plasma renin in rats receiving enalapril. None of these findings could be explained by changes in the ratio of active and inactive renin. Water diuresis, without natriuresis and with a decrease in potassium urinary excretion, occurred with the higher dose of enalapril. Enalapril did not potentiate the elevation of PRA in two-kidney one-clip Goldblatt hypertensive rats. In conclusion, enalapril produced renin secretion, which was in part β-adrenergically mediated. The negative short feedback loop of angiotensin II and prostaglandins did not appear to be involved. A vasodilator effect, apparently independent of ACE inhibition, was found in intact conscious sodium-replete rats.

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