The Activities of 1-Hydrazinophthalazine (Ba-5968), a Hypotensive Agent*

Craver, Bradford N.; Barrett, W. E.; Cameron, A; Yonkman, Fredrick F.

doi:10.1002/jps.3030401109

Cited by 42 publications

(16 citation statements)

References 4 publications

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“…The dose of each drug was comparable to previously published effective doses (8,10,23). The dose was determined by titrating each agenGo the maximum fall in systemic resistance without changing Ao in two preliminary lambs.…”

Section: Discussionsupporting

confidence: 75%

“…Larger doses of hydralazine or minoxidil caused2 further reduction in Rs but also caused sharp reductions in Ao (data not shown). The qualitative effects of these agents are not dose dependent (8,10,23) and there was no qualitative change following bolus administration in this study. Thus, it is unlikely that the observed pattern of response for each drug would be dose dependent.…”

Section: Discussionmentioning

confidence: 55%

“…Hydralazine was given in a dose of 0.75 mg/kg and the intravenous preparation was obtained from the hospital pharmacy. The approximate dose for each drug was determined from published values (8,10,23). The dose was then adjusted in initial studies in two l a m b t o produce the maximum reduction in R, without changing Ao.…”

Section: Methodsmentioning

confidence: 99%

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Vasodilators and Ventricular Septal Defect: Comparison of Prazosin, Minoxidil, and Hydralazine in a Chronic Lamb Model

1984

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SummaryThe volume overloading of the left ventricle which results from left to right (L-R) shunting through a ventricular septal defect (VSD) may be reduced by pharmacologic agents which lower systemic vascular resistance (R,) in excess of pulmonary arteriolar vascular resistance (R,). To study agents capable of decreasing the L-R shunt through systemic vasodilatation, we created a chronic lamb model with VSD and administered three vasodilators, prazosin (0.05 mg/kg), hydralazine (0.75 mg/kg), and minoxidil (0.25 mg/kg). Prazosin increased the R, while lowering R,, resulting in an increase in R,/R by 43% ( p Q 0.005). Prazosin decreased the pulmonary flow (Q,) slightly, decreased L-R shunt by 16%, reduced the pulmonary to systemic flow ratio Received July 25, 1983; accepted February 7, 1984 (QP/QS) b c 2 % ( p Q 0.005), and lowered the left atrial mean pressure (LA) by 16% ( p s 0.005) with no effect on heart rate.Hydralazine lowered the R, and R, equally and thus did not change the R,/R, or the v o l s e of L-R shunt (7.6 versus 8.1 liters/min/m2). No change in LA was seen with hydralazine but heart rate increased from 162 to 200/min (p 4 0.01). Minoxidil did not change the L-R shunt (6.9 versus 6.8 liters/min/m2) and, in general, produced effects intermediate between prazosin and hydralazine. The data support a selective systemic vasodilation with prazosin, a property not shared by either minoxidil or hydralazine, which results in a reduction of shunting and left ventricular volume overloading in lambs with VSD. Furthermore, since prazosin did not decrease the pulmonary resistance, the data indicate that the elevation in pulmonary resistance in lambs with VSD is not mediated by the a,-adrenergic receptor. Abbreviations VSD, ventricular septal defect R, , pulmonary arteriolar vascular resistance

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Section: Discussionsupporting

confidence: 75%

Section: Discussionmentioning

confidence: 55%

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Vasodilators and Ventricular Septal Defect: Comparison of Prazosin, Minoxidil, and Hydralazine in a Chronic Lamb Model

1984

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“…In animals given larger doses than those used clinically in man the drug moderates but does not block epinephrine and norepinephrine hypertension nor does it produce epinephrine reversal. [18][19][20] In the present study there appeared to be slight inhibition of the norepinephrine but not the epinephrine pressor response. However, the most striking observation was the marked inhibition of the bradyeardia induced by norepinephrine.…”

Section: Discussionmentioning

confidence: 56%

The Effect of "Sympatholytic Drugs on the Cardiovascular Responses to Epinephrine and Norepinephrine in Man

1951

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Under controlled conditions the effects of various "sympatholytic" agents on the cardiovascular responses to epinephrine and norepinephrine were compared in man. The dosages of the sympatholytic drugs administered approximated those usually employed clinically. Such basic data are given for the following agents: Dibenamine, the imidazoline derivatives [Priscoline and Regitine (C-7337)], the dihydrogenated alkaloids of ergot (D.H.K. and C.C.K.), L-hydrazinophthalazine (C-5968), tetraethylammonium, and hexamethonium (C6).

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“…1-Hydrazinophthalazine has been demonstrated to cause a fall in peripheral artery pressure, to possess slight adrenergic blocking properties, to increase renal plasma flow (1)(2)(3)(4)(5)(6)(7)(8), and to cause a proportional increase in cardiac output (8). It has been stated that the cardio-stimulating effects of 1-hydrazinophthalazine are mediated via the autonomic nervous system, since they can be blocked by sympathectomy or ganglionic blockade (9,10).…”

mentioning

confidence: 99%

Cardiovascular and Renal Responses to the Combination of Hexamethonium and 1-Hydrazinophthalazine (Apresoline®) in Hypertensive Subjects1

Stein¹,

Hecht²

1955

J. Clin. Invest.

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The Activities of 1-Hydrazinophthalazine (Ba-5968), a Hypotensive Agent*

Cited by 42 publications

References 4 publications

Vasodilators and Ventricular Septal Defect: Comparison of Prazosin, Minoxidil, and Hydralazine in a Chronic Lamb Model

Vasodilators and Ventricular Septal Defect: Comparison of Prazosin, Minoxidil, and Hydralazine in a Chronic Lamb Model

The Effect of "Sympatholytic Drugs on the Cardiovascular Responses to Epinephrine and Norepinephrine in Man

Cardiovascular and Renal Responses to the Combination of Hexamethonium and 1-Hydrazinophthalazine (Apresoline®) in Hypertensive Subjects1

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