[Comparative evaluation of prostaglandins E1 and E2 in patients with hypertension]. / Sravnitel'naia otsenka deistviia prostaglandinov E1 i E2 u bol'nykh gipertonicheskoi bolezn'iu.

Changes in ABP, ECG, cerebral and peripheral hemodynamics were examined in 29 patients with second-stage essential hypertension before and within 1 or 2 days after PGE1 and PGE2 infusions administered during follow-up or in the presence of a hypotensive therapy. PGE were shown to be active vasodilators increasing cerebral and peripheral circulation. Vascular PG effects persisted for 1 or 2 days after the administration. Hypertensive patients demonstrated two patterns of hemodynamic response to PGE. The patients with higher total peripheral resistance (TPR) and low stroke and cardiac indices (SI and CI) during follow-up or hypotensive treatment were more sensitive to PGE, their ABP falling because of declining TPR. The patients with high SI and normal or slightly elevated TPR were less sensitive to PGE, their ABP falling mostly at the expense of declining SI. Most patients showed changed end portion of the ventricular complex immediately after PGE administration that vanished within one or two days. In coronary patients, angina of effort occurred less frequently after PGE infusion.

[Renal prostaglandins and hypertension]. / Prostaglandiny pochek i gipertonicheskaia bolezn'.

A total of 154 patients with essential hypertension (EH), 24 patients with renovascular hypertension (RVH), and 130 Wistar rats were investigated. PGE2 and PGF2 alpha levels were assayed radioimmunologically in renal venous blood and urine of the patients, and the synthesis of PGE2 and PGF2 alpha in renal tissue, renal PGE-9-ketoreductase activity and urinary PG excretion were measured in rats. It was demonstrated that the PGE2 synthesis was depressed in the vascular channel and the renal uropoietic system, with elevated F/E rations, in patients with arterial hypertension. Clinical and experimental studies showed prolonged and excessive salt consumption to be a cause of these changes, rooted in suppressed renal biosynthesis of both PGs and increased conversion of PGE2 to PGF2 alpha. In addition, renal PGE2 inactivation was increased in EH patients, as compared to those with RVH. PGE2 produced in the kidneys of EH patients is always a depressor natriuretic substance, whereas the role of PGF2 alpha is dependent on the water-salt balance. Furosemide and, to a smaller extent, other diuretics, as well as some hypotensive agents, increase urinary PG excretion and depress the F/E ratio in the urine. Repeated PGE2 infusions are shown to enhance the sensitivity of EH patients to hypotensive drugs, so they can be used for the treatment of refractory EH cases.

[Use of series E prostaglandins in the treatment of essential hypertension]. / Ispol'zovanie prostaglandinov serii E dlia lecheniia bol'nykh gipertonicheskoi bolezn'iu.

Fifty-four hypertensive patients with the average BP level of 208 +/- 3.2/125 +/- 2.4 mm Hg were infused 2 doses of PGE. Forty patients received PGE2 in the form of protein (USA) and 14 patients were administered PGE1 in the form of alprostadil (USA). Each patient received on the average 3.5 mg of PGE2 or 0.7 mg of PGE1 during 48 hours. PGE infusion by the devised scheme induced no significant side-effects, was attended by an increase in the diuresis and natriuresis as well as a BP decrease (more pronounced with PGE1) not only in the period of the infusion but also during the 2-3 days following it. The hypotensive effect and BP fall in the orthostatic position were more marked following PGE2 infusion. PGE enhanced the sensitivity of the patients to obsidan, clophelin, hydrochlorothiazide and to a lesser degree to corinfar. Infusion of PGE2 to patients with essential hypertension resistant to hypotensive agents reduced the BP and made it possible to diminish the number of the drugs prescribed and their doses. The hypotensive effect of the drugs administered persisted for up to 5-7 months. It can be expected that repeated infusions of PGE2 every 6 months, will contribute to an alleviation of arterial hypertension, the patient's clinical improvement and the lowering of doses of hypotensive drugs.