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.

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

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.

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

1984 ◽  
Vol 62 (1) ◽  
pp. 116-123 ◽  
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.

Renal sodium handling in normal humans subjected to low, normal, and extremely high sodium supplies

1985 ◽  
Vol 249 (6) ◽  
pp. F941-F947 ◽  
Author(s):  
J. C. Roos ◽  
H. A. Koomans ◽  
E. J. Dorhout Mees ◽  
I. M. Delawi
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Sodium Intake ◽  
Extracellular Fluid ◽  
Plasma Renin ◽  
Renin Activity ◽  
Sodium Reabsorption ◽  
Lithium Clearance ◽  
Renal Sodium Handling ◽  
Sodium Handling

We studied renal sodium handling, extracellular fluid volume (ECFV), plasma renin activity, aldosterone and norepinephrine, and blood pressure in eight healthy volunteers after equilibration on intakes of 20, 200, and 1,128 +/- 141 meq sodium, respectively. Renal sodium handling was assessed by means of clearance studies during maximal water diuresis and lithium clearance. Urinary sodium excretions were 22 +/- 4, 202 +/- 19, and 1,052 +/- 86 meq/day. From the lower to the upper sodium intake level, 24-h creatinine clearance rose from 111 +/- 7 to 136 +/- 11 ml/min and inulin clearance from 103 +/- 9 to 129 +/- 9 ml/min, whereas proximal and distal fractional sodium reabsorption (FSRprox and FSRdist, respectively) fell from 86.8 +/- 1.3 to 79.0 +/- 2.7% and from 96.5 +/- 0.5 to 76.0 +/- 1.9%, respectively. During the normal sodium intake (200 meq), intermediate values were recorded. The changes in fractional lithium clearance were less consistent but correlated with FSRprox (r = 0.78, P less than 0.001) and not with FSRdist. Major changes in plasma renin activity, aldosterone, and, to a lesser extent, norepinephrine accompanied these changes in kidney function, displaying inverse and exponential correlations with daily sodium excretion and ECFV. No consistent rise in blood pressure was detected. These observations indicate that in healthy humans renal adaptation to vast variations in sodium intake includes resetting of glomerular filtration rate, FSRprox, and, in particular, FSRdist. Alterations in neurohumoral factors may play a dominant role in this adaptation.

Hypertension in Dahl salt-sensitive rats: biochemical and immunohistochemical studies

1992 ◽  
Vol 83 (1) ◽  
pp. 13-22 ◽  
Author(s):  
J. Bouhnik ◽  
J. P. Richoux ◽  
H. Huang ◽  
F. Savoie ◽  
T. Baussant ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
High Salt ◽  
Renin Activity ◽  
Deficient Diet ◽  
High Salt Diet ◽  
Salt Diet ◽  
Plasma Angiotensin

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.

Relationship between the Hypotensive and Renin-Stimulating Actions of Diuretic Therapy in Hypertensive Patients

1978 ◽  
Vol 55 (s4) ◽  
pp. 307s-309s ◽  
Author(s):  
G. Leonetti ◽  
Laura Terzoli ◽  
Carla Sala ◽  
C. Bianchini ◽  
Laura Sernesi ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Diuretic Therapy ◽  
Plasma Renin ◽  
Hypotensive Effect ◽  
Renin Activity ◽  
Hypotensive Activity ◽  
Pressor Responses ◽  
Angiotensin Ii Antagonist

1. The pressor role of renin stimulated by chronic diuretic therapy has been assessed in 31 patients with essential hypertension by infusing the angiotensin II antagonist, saralasin, immediately before and at the end of 2 weeks' treatment with the diuretic, chlorthalidone. 2. Under diuretic therapy the change in blood pressure caused by saralasin was found to be correlated to plasma renin activity values, in such a way that small pressor responses were again observed in patients whose renin was mildly stimulated by the diuretic, whereas a marked depressor response occurred in patients whose renin was markedly increased. 3. On the other hand, the hypotensive effect of chlorthalidone was correlated to values of plasma renin activity under diuretic therapy in an opposite direction: indeed little or no decrease and sometimes an increase in blood pressure were observed in patients with marked renin activation by diuretic therapy. 4. It is concluded that stimulation of renin release by chronic diuretic therapy can be considered a factor limiting the hypotensive activity of diuretic drugs.

Plasma Renin in Long-Term Diuretic Treatment of Hypertension: Effect of Discontinuation and Restarting Therapy

1982 ◽  
Vol 63 (2) ◽  
pp. 121-125 ◽  
Author(s):  
S. Swart ◽  
R. F. Bing ◽  
J. D. Swales ◽  
H. Thurston
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Juxtaglomerular Apparatus ◽  
Significant Rise ◽  
Renin Activity ◽  
Hypertensive Patients ◽  
Diuretic Treatment ◽  
Low Renin Hypertension ◽  
Before And After

1. Plasma renin activity, body weight and blood pressure were measured before and after 7 days' treatment with bendrofluazide in ten hypertensive subjects. They were then treated with bendrofluazide alone (5 mg daily) for a minimum of 3 years. The diuretic was then discontinued and the measurements were repeated before and again after 7 days with bendrofluazide. The results were compared with those obtained before chronic treatment with the diuretic. 2. Chronic diuretic treatment was associated with a persistent and progressive rise in plasma renin activity, that fell promptly to pretreatment levels when diuretics were discontinued. This was associated with significant weight gain but no immediate significant rise in blood pressure. 3. When acutely challenged with bendrofluazide the patients showed a greater increase in plasma renin activity on the second occasion than on the first. Three out of five patients with an initially subnormal response had normal responses after chronic diuretic treatment. 4. Chronic diuretic treatment increased the responsiveness of the juxtaglomerular apparatus in some hypertensive patients. 5. Classification of hypertensive patients into renin subgroups may be influenced by previous therapy, even when that therapy has been discontinued for 4 weeks. In particular ‘low renin hypertension’ may be masked by recent use of diuretics, as shown by three of the five patients in this subgroup in the present study.

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

1988 ◽  
Vol 75 (3) ◽  
pp. 293-300 ◽  
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.

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

1976 ◽  
Vol 41 (3) ◽  
pp. 323-327 ◽  
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.

Effect of Angiotensin II and Converting Enzyme Inhibitor (Captopril) on Blood Pressure, Plasma Renin Activity and Aldosterone in Primary Aldosteronism

1981 ◽  
Vol 61 (s7) ◽  
pp. 289s-293s ◽  
Author(s):  
F. Mantero ◽  
F. Fallo ◽  
G. Opocher ◽  
D. Armanini ◽  
M. Boscaro ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Primary Aldosteronism ◽  
Enzyme Inhibitor ◽  
Plasma Renin ◽  
Renin Activity ◽  
Converting Enzyme ◽  
Converting Enzyme Inhibitor ◽  
Idiopathic Hyperaldosteronism

1. Patients with idiopathic hyperaldosteronism (IHA) show a response of aldosterone to posture which is not present in patients with aldosterone-producing adenoma (APA). We have determined whether this could be explained by a different sensitivity to angiotensin II. 2. Angiotensin II was infused in gradually increasing doses in six patients with APA and in seven patients with IHA. No changes in aldosterone concentration were found at the end of each period in APA, whereas there was a significant increase in IHA; blood pressure rose by a similar extent in both groups. 3. In order to evaluate the role of endogenous angiotensin II, captopril, a converting enzyme inhibitor, was administered to six patients with APA and five patients with IHA at a dose of 75 mg/day for 1 week. There was a significant fall of mean blood pressure in IHA and only minimal changes in APA. Plasma renin activity and plasma and urinary aldosterone were unchanged in APA. In IHA there was a small increase in upright plasma renin activity and a slight decrease in both plasma and urinary aldosterone, but these changes were not significant. 4. These findings further support the idea that idiopathic hyperaldosteronism is a clinical state different from that occurring in primary aldosteronism due to adenoma, and may be more closely related to essential hypertension.

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