By M. M. Winbury (auth.), Professor Dr. P. R. Lichtlen, Priv.-Doz. Dr. H.-J. Engel, Dr. A. Schrey, Dr. H. J. C. Swan (eds.)

Pharmacological and scientific learn on nitrates is still of becoming curiosity in lots of facilities. this is often incredible in view of the truth that their favorable results in angina pectoris have been defined via Brunton and via Murrell within the Lancet greater than a hundred years in the past. As anticipated, a bunch of recent details has been accrued because the prior symposia on nitrates held in Stockholm in 1975 and Berlin in 1978. New insights have been received into the pharmacology, pharmacokinetics and pharmacodynamics of nitrates, in addition to into their medical results in acute and protracted ischemic center illnesses and in serious congestive middle failure. particularly little development, even if, was once saw in examine into the fundamental motion of nitrates. even though such a lot investigators agree that intracellular sequestration of calcium is one of the major mechanism during which nitrates result in the relief of vascular tender muscle tone, the precise web site in their motion nonetheless continues to be undefined. against this, dose-dependent adjustments in venous and arteriolar tone have lengthy been basically confirmed. therapy was once back basically movement of dialogue. The query of tolerance following long term management was once mentioned extensive and the time period "pseudotolerance" was once brought to explain the difference of the body's circulatory process to continual vasodilation. this can be in particular vital in long-term prophylactic antiischemic therapy in reliable, in addition to in risky angina pectoris (i.e. in the course of elevated vasomotor tone - spasm).

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5. Temporal variation of the mean DPG systolic amplitude response intensity for 12 healthy male volunteers dosed sublingually with nitroglycerin. 9mg NTG ing dose-effect curve is presented in Fig. 6. 9 mg. 8 mg (Warner-Lambert) sublingual nitroglycerin. Each point plotted in Fig. 7 has been converted to relative biophasic drug levels, using the dose-effect curve shown in Fig. 6 in a manner described in detail elsewhere [2-5, 7]. The resulting values have been normalized by dividing by the dose and replotted as dose-normalized relative biophasic drug levels in Fig.

Time course of plasma isosorbide dinitrate (ISDN) concentration after 15, 30, 60, and 120 mg ofISDN administered acutely and during sustained therapy. Data represent mean values ±SD. OI) Table 1. Effects of placebo and isosorbide dinitrate (ISDN) during acute and sustained therapy on standing systolic blood pressure a Drug Hours after dose 0 2 4 6 Placebo A S 137 ± 15 133±15 135± 10 130± 15 135± 10 129± 12 135± 15 133 ± 12 133 ± 12 131 ± 12 ISDN 15mg A S 145± 17 137 ± 17 106±20 b 122± 15 c 117±20 b 128±17 c 116± 15 b 131 ± 17 ISDN 30mg A S 140± 15 135± 15 113±17 b 116±22 c 101 ± 15 b 114± 12 d 113±22 b 123± 15 d ISDN 60mg A S 137± 12 139± 17 99±22 b 118± 15 b 98± 12b 115± IO d 92±22 b 113 ± 12 b 101 ± 7 b 125± 17 d 113±20 b 132±20 103±15 b 133± 17 ISDN 120mg A S 134± 10 139± 17 91± 17 b 118±17 d 88± 17 b 115± 15 d 93±20 b 128± 15 c 98±17 b 130± 17 a Values are mean ± SD.

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