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EFFECTS OF 1‐SAR‐8‐ALA‐ANGIOTENSIN II ON SYSTEMIC AND PULMONARY HAEMODYNAMICS IN HYPERTENSIVE PATIENTS
Author(s) -
Fagard R.,
Amery A.,
Lijnen P.,
Reybrouck T.,
Joossens J.V.,
Billiet L.,
Moerman E.,
Schaepdryver A.
Publication year - 1978
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1978.tb00697.x
Subject(s) - saralasin , medicine , vascular resistance , angiotensin ii , blood pressure , pulmonary wedge pressure , cardiac output , sodium , cardiology , endocrinology , chemistry , organic chemistry
SUMMARY 1.The angiotensin II antagonist, 1‐Sar‐8‐Ala‐angiotensin II (saralasin), was infused intravenously at a rate of 10 μg/kg per min in thirty‐three hypertensive patients, on a normal sodium diet (130 mmol per day) and/or during sodium depletion by low sodium diet (20 mmol per day) and chlorthalidone. 2. In both series, saralasin induced a transient rise in intra‐arterial pressure ( P < 0.01), accompanied by a slight decrease in heart rate ( P < 0.01). The elevation of systolic arterial pressure reached its maximum after 4 min and was more pronounced in sodium‐replete patients. Plasma noradrenaline was significantly elevated by 29.7% ( P <0.01), but the rise in pressure was not related to concomitant changes in plasma noradrenaline. 3. After the initial pressor effect, arterial pressure, heart rate, cardiac output and total peripheral resistance remained unchanged in the sodium‐replete patients, while in the sodium‐depleted conditions mean arterial pressure and peripheral resistance were reduced, by 17.8% and 18.6% ( P < 0.001) respectively, within 60min. Reflex increases in heart rate (+3.8%) and cardiac output (+ 11.1%) occurred after 10 min ( P <0.05), but were not sustained thereafter. 4. Pulmonary vascular resistance was not affected by saralasin. In sodium‐depleted patients, pulmonary capillary wedge pressure decreased by 1.2mmHg ( P <0.01), with parallel changes of pulmonary artery pressure ( P < 0.01).