scholarly journals Plasma vasopressin and blood pressure. Studies in normal subjects and in benign essential hypertension at rest and after postural challenge.

Heart ◽  
1983 ◽  
Vol 49 (6) ◽  
pp. 528-531 ◽  
Author(s):  
R Davies ◽  
M Forsling ◽  
G Bulger ◽  
T Phillips
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Normal Subjects ◽  
Plasma Vasopressin ◽  
Postural Challenge

Effect of Intravenous Frusemide on Plasma Renin Concentration: Suppression of Response in Hypertension

1975 ◽  
Vol 49 (4) ◽  
pp. 353-358 ◽  
Author(s):  
P. L. Padfield ◽  
M. E. M. Allison ◽  
J. J. Brown ◽  
A. F. Lever ◽  
R. G. Luke ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
High Blood Pressure ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Primary Hyperaldosteronism ◽  
Plasma Renin Concentration ◽  
Low Renin Hypertension ◽  
Renal Adaptation

1. Intravenous frusemide produced in normal subjects a prompt rise of plasma renin concentration which correlated with urinary sodium. 2. The renin response to frusemide was suppressed in patients with primary hyperaldosteronism. 3. In patients with low-renin hypertension and normal renin essential hypertension, the renin response to frusemide was similarly suppressed. 4. Suppression of the renin response to frusemide is therefore a feature of hypertension not confined to patients with primary hyperaldosteronism and low-renin hypertension. 5. Thus low-renin hypertension does not appear to constitute a distinct diagnostic entity. 6. It is suggested that suppression of the renin response is part of a long-term renal adaptation to high blood pressure.

Angiotensin II Blockade in Normal Subjects and Essential Hypertensive Patients

1976 ◽  
Vol 51 (s3) ◽  
pp. 193s-196s
Author(s):  
G. A. MacGregor ◽  
P. M. Dawes
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Angiotensin Ii ◽  
Sodium Intake ◽  
Normal Subjects ◽  
Competitive Inhibitor ◽  
Hypertensive Patients ◽  
Sodium Diet ◽  
Incremental Rate ◽  
Standing Blood Pressure

1. Saralasin (Sar1-Ala8-angiotensin II), a competitive inhibitor of angiotensin II (AII), has been infused into normal subjects and patients with essential hypertension when deprived of sodium by 5 days of a 10 mmol/day sodium diet. 2. When saralasin was given by an incremental rate of infusion starting at 0·25 μg min—1 kg—1, sodium-deprived normal subjects showed a fall in standing blood pressure with no change in lying blood pressure, sodium-deprived normal-renin hypertensive patients showed no change in lying or standing blood pressure and sodium-deprived low-renin patients showed a significant sustained rise in lying and standing blood pressure. 3. These findings suggest that: (a) standing blood pressure in sodium-deprived normal subjects is angiotensin II dependent; (b) normal-renin hypertensive patients when sodium deprived by diet alone do not appear to be angiotensin II dependent (angiotensin II is unlikely therefore to be directly maintaining their blood pressure on their normal sodium intake); (c) the rise in blood pressure seen in low-renin hypertensive patients with saralasin may be a further way of distinguishing this group of patients.

Acute Effects of Captopril on Blood Pressure and Circulating Hormone Levels in Salt-Replete and Depleted Normal Subjects and Essential Hypertensive Patients

1981 ◽  
Vol 61 (1) ◽  
pp. 75-83 ◽  
Author(s):  
J. A. Millar ◽  
B. P. McGrath ◽  
P. G. Matthews ◽  
C. I. Johnston
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Pulse Rate ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Primary Role ◽  
Ang Ii ◽  
Acute Effects ◽  
Mean Values ◽  
Plasma Renin Concentration

1. The acute effects of a single oral dose of captopril on blood pressure, pulse rate and circulating levels of angiotensin I (ANG I), angiotensin II (ANG II), renin, bradykinin and catecholamines were studied in three groups: eight normal subjects, six salt-depleted normal subjects and 16 patients with essential hypertension. 2. Captopril treatment did not cause any significant fall in supine blood pressure in salt-replete normal subjects or patients with untreated essential hypertension but was associated with a fall in mean blood pressure from 85 ± 2 to 75 ± 2 mmHg in salt-depleted normal subjects and from 131 ± 7 to 117 ± 5 mmHg in patients with essential hypertension treated with diuretics. There was no change in pulse rate in any group. 3. Hormonal responses to captopril were qualitatively similar in the three groups and consisted of significant falls in ANG II with corresponding increases in ANG I and plasma renin concentration. The changes in plasma renin concentration and ANG I were greater in salt-depleted normal subjects (mean values at 90 min were 1140% and 990% of basal levels respectively) than in salt-replete normal subjects (410%, 190%) and were blunted in patients with essential hypertension (140%, 120%). Blood bradykinin, noradrenaline and adrenaline concentrations did not change after captopril in any group. 4. The parallel fall in blood pressure and ANG II levels in salt-depleted normal subjects is consistent with maintenance of blood pressure by increased levels of ANG II in sodium depletion. 5. The failure of captopril to reduce acutely blood pressure in patients with essential hypertension despite suppression of plasma ANG II and without change in circulating bradykinin confirms that the renin-angiotensin system does not play a primary role in essential hypertension.

Interaction of Dopamine, Methyldopa and Reserpine in the Sympatho-Adrenal System in Essential Hypertension

1976 ◽  
Vol 51 (s3) ◽  
pp. 461s-463s
Author(s):  
K. Abe ◽  
H. Aoyagi ◽  
M. Yasujima ◽  
S. Miyazaki ◽  
T. Kusaka ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Peripheral Nerve ◽  
Pressor Response ◽  
Normal Subjects ◽  
Term Treatment ◽  
Adrenal System ◽  
Long Term Treatment ◽  
Depressor Effect

1. The interactions of dopamine, reserpine and methyldopa on blood pressure of normal subjects and of those with essential hypertension were examined. 2. When biosynthesis of noradrenaline from dopamine was blocked by reserpine, dopamine induced a prominent depressor effect in essential hypertension. 3. The long-term treatment with methyldopa induced a marked potentiation of the pressor action of domapine in hypertension, although no significant pressor response was found in normal subjects. 4. It is suggested that methylnoradrenaline may accumulate in peripheral nerve endings of patients with essential hypertension in comparison with normal subjects, and this accumulated methylnoradrenaline potentiates the pressor response to dopamine in essential hypertension.

High-Renin Essential Hypertension: Adrenergic Cardiovascular Correlates

1976 ◽  
Vol 51 (s3) ◽  
pp. 181s-184s ◽  
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.

Plasma Catecholamines and the Pressor Response to Sar1-Ala8-Angiotensin II in Man

1977 ◽  
Vol 53 (4) ◽  
pp. 341-348
Author(s):  
B. P. McGrath ◽  
J. G. G. Ledingham ◽  
C. R. Benedict
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Angiotensin Ii ◽  
Pressor Response ◽  
Plasma Catecholamines ◽  
Normal Subjects ◽  
Plasma Noradrenaline ◽  
Dialysis Patients ◽  
Anephric Patients ◽  
Change In Mean

1. The initial blood pressure response to saralasin (Sar1-Ala8-angiotensin II) infusion was examined in 15 normal subjects, eight patients with untreated essential hypertension and 65 patients established on chronic haemodialysis (including six anephric patients), and related to measurements of plasma renin activity (PRA), angiotensin II, plasma catecholamines (noradrenaline and adrenaline), blood volume and extracellular fluid volume ([35S]sulphate space or exchangeable sodium). 2. A transient rise in arterial pressure, maximum after 5–6 min, occurred in all normal subjects, patients with essential hypertension and anephric patients, and in 41 of the 59 dialysis patients with kidneys. 3. In the normal subjects, saralasin infusion resulted in a significant rise in plasma noradrenaline (mean increase 360%, P < 0·02) without change in plasma adrenaline concentration. The change in noradrenaline was significantly related to the change in mean blood pressure (P < 0·05) and was similar to the response to 5 min of a 40° head-up tilt. 4. An increase in plasma noradrenaline also occurred in dialysis patients (P < 0·005) but the change in mean blood pressure with saralasin in this group was inversely related to PRA (P < 0·001) and angiotensin II (P < 0·001), directly related to blood volume (P < 0·001), but unrelated to the change in plasma noradrenaline. 5. The pressor response to saralasin may be mediated not only by angiotensin-like action on vascular receptors but also by an action on the central or peripheral autonomic nervous system.

Abnormalities and Drug-Induced Alterations of Vasopressin in Human Hypertension

1981 ◽  
Vol 61 (s7) ◽  
pp. 149s-152s ◽  
Author(s):  
M. Thibonnier ◽  
J. C. Aldigier ◽  
M. E. Soto ◽  
P. Sassano ◽  
J. Menard ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Antihypertensive Drugs ◽  
Blood Pressure Reduction ◽  
Normal Subjects ◽  
Pressure Reduction ◽  
Drug Induced ◽  
Vasopressin Release ◽  
Hypertensive Patients ◽  
Plasma Vasopressin ◽  
Captopril Treatment

1. Plasma vasopressin was estimated in 20 normotensive, 46 moderate hypertensive and 14 severe hypertensive patients under normal sodium diet. 2. In moderate hypertensive patients basal values for plasma vasopressin (PVP) after overnight dehydration and 24 h urinary vasopressin (UVP) were respectively 1.82 ± 0.23 pmol/l and 44 ± 4 pmol/day, which were not different from those found in normal subjects (PVP = 1.14 ± 0.11 pmol/l and UVP = 54 ± 4 pmol/day). In contrast, basal values were significantly increased in severely hypertensive patients (PVP = 4.69 ± 1.45 pmol/l, P &lt; 0.005; UVP = 107 ± 17 pmol/day, P &lt; 0.01). 3. In a group of 12 moderately hypertensive patients the blood pressure reduction induced by a single 20 mg dose of nifedipine was associated with an increase in PVP from 1.48 ± 0.57 to 2.48 ± 0.74 pmol/l (P &lt; 0.05) and in UVP from 42 ± 7 to 67 ± 17 pmol/day (P &lt; 0.05). On the other hand, a single dose of captopril (1 mg/kg body weight) administered to the same patients did not alter PVP (1.68 ± 0.43 pmol/l) and UVP (40 ± 6 pmol/day) despite a similar blood pressure decrease. 4. In a group of 10 severely hypertensive patients, the blood pressure reduction induced by the first dose of captopril (1 mg/kg) was correlated to the pretreatment level of PVP (r = 0.89, P &lt; 0.001) and of UVP (r = 0.70, P &lt; 0.01). Eight days of captopril treatment reduced PVP from 5.24 ± 1.38 to 1.18 ± 0.32 pmol/l (P &lt; 0.01) and UVP from 68 ± 17 to 25 ± 3 pmol/day (P &lt; 0.001). 5. Increased levels of vasopressin are a marker of severe forms of hypertension. The reduction of vasopressin during captopril treatment could be an additional mechanism underlying the anti-hypertensive effect of that drug. Moreover, from the comparison between nifedipine and captopril, it appears that antihypertensive drugs have different effects on vasopressin release.

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