1. Cardiovascular responses to isometric exercise and standing in normotensive subjects during converting enzyme inhibition with teprotide
A P Niarchos, T G Pickering, J H Laragh Hypertension . 1982 Jul-Aug;4(4):538-44. doi: 10.1161/01.hyp.4.4.538.
The hemodynamic responses to isometric exercise (hand grip) were investigated in normotensive subjects during a 150 mEq (n = 8) sodium diet and a 10 mEq (n = 6) sodium diet both before and after the administration of the converting enzyme inhibitor teprotide. Although teprotide significantly decreased the mean arterial pressure during both sodium intakes, the normal pattern of hemodynamic response to hand grip was preserved, that is mean arterial pressure was increased by hand grip mainly because of an increase in cardiac output. Changes of plasma catecholamines during hand grip were not affected by teprotide. In addition, the hemodynamic responses to standing were not substantially altered by teprotide. When fainting occurred (in the seated position) following the administration of teprotide, it was associated not only with a decrease in arterial pressure but also with a concurrent reduction in cardiac output. We conclude that angiotensin inhibition by teprotide does not significantly impair sympathetically mediated cardiovascular responses.
2. Hormonal and blood pressure changes during converting enzyme inhibition by teprotide
M J VandenBurg, V L Sharman, J J Morton, F P Marsh, G H Williams Postgrad Med J . 1981 May;57(667):283-8. doi: 10.1136/pgmj.57.667.283.
Changes induced by i.v. and subcutaneous teprotide in plasma renin, angiotensin I, angiotensin II, aldosterone and bradykinin were studied in a renal transplant patient with severe high renin hypertension, before and after trinephrectomy. The immediate reduction in BP produced by teprotide was not solely attributable to the inhibition of conversion of angiotensin I to angiotensin II, because there was also a transient increase in serum bradykinin; however, the prolonged antihypertensive effect of teprotide appeared independent of bradykinin. After trinephrectomy, teprotide lowered systolic BP but had no significant effect on diastolic BP or plasma bradykinin. beta-Blockade prevented the secondary increase in plasma renin which followed teprotide, thereby potentiating its anti-hypertensive effect.
3. Drug-induced hyperkalemia
A B Schwartz, M L Cannon-Babb Hosp Pract (Off Ed) . 1986 Sep 30;21(9A):99-107, 111, 114-27.
This is the era of polypharmacy. Treatment with multiple therapeutic agents for multiple underlying medical conditions leads to greater vulnerability to such metabolic imbalances as hyperkalemia. The physician must know which underlying medical conditions and drugs predispose to abnormal intracellular-extracellular potassium balance and abnormal regulation of potassium excretion.
