Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Nitroprusside”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 235 records · Page 13Linked to original sources
PubMed2003

Inhibition of high K+-evoked gamma-aminobutyric acid release by sodium nitroprusside in rat hippocampus.

To clarify whether nitric oxide (NO) modifies high K(+)-evoked gamma-aminobutyric acid (GABA) release, we examined the effects of sodium nitroprusside, an NO donor; diethyldithiocarbamate, an NO trapper; dithiothreitol, a superoxide radical scavenger; and 1H-(1,2,4)oxadiazole(4,3-a)quinoxalin-1-one, a specific guanylyl cyclase inhibitor, on high (100 mM) K(+)-evoked GABA release from rat hippocampus in vivo using microdialysis. Perfusion with 0.5 or 5 mM sodium nitroprusside significantly reduced high K(+)-evoked GABA release. Co-perfusion with 0.5 mM sodium nitroprusside and 5 mM diethyldithiocarbamate or 0.5 mM 1H-(1,2,4)oxadiazole(4,3-a)quinoxalin-1-one significantly enhanced high K(+)-evoked GABA release. Co-perfusion with 0.5 mM sodium nitroprusside and 1 mM dithiothreitol tended to increase it. These results demonstrate that sodium nitroprusside reduces high K(+)-evoked GABA release both via an NO/cyclic GMP-dependent pathway and via an NO-dependent, but cyclic GMP-independent, pathway in rat hippocampus in vivo.

Animals↗
PubMed1998

Involvement of GABA and glutamate receptors in the blood pressure responses to intrathecally injected sodium nitroprusside in anesthetized rats.

In pentobarbital-anesthetized rats the intrathecal (i.t.) injection of the nitric oxide (NO) donor, sodium nitroprusside (125, 250 and 500 nmol), induced a dose-dependent hypotensive response followed by a dose-dependent pressor effect. The pressor response to sodium nitroprusside (250 nmol) was reduced to 30% of the control value by the selective antagonist for AMPA/kainate receptors, 6.7-dinitroquinoxaline-2,3-dione (50 nmol, i.t.), whereas it was not modified by the selective NMDA receptor antagonist, 2-amino-5-phosphono-valeric acid (30 nmol, i.t.). The hypotensive effect of sodium nitroprusside was antagonized by the GABA(A) receptor antagonists, bicuculline (4.4 nmol, i.t.) and picrotoxin (4.4 nmol, i.t.), and also by the GABA(B) receptor antagonist, 2-hydroxy saclofen (113 nmol, i.t.). The blood pressure responses to sodium nitroprusside were not modified by blockade of muscarinic receptors with methyl atropine (164 nmol, i.t.), or of nicotinic receptors with hexamethonium (211 nmol, i.t.), of alpha1-adrenoceptors with prazosin (3.1 nmol, i.t.), of alpha2-adrenoceptors with yohimbine (2.8 micromol/kg, i.v.), of 5-HT receptors with methysergide (5.1 micromol/kg, i.v.), or of glycine receptors with strychnine (65 nmol, i.t.). It is concluded that NO generated from sodium nitroprusside in the spinal cord exerts inhibitory and excitatory effects on blood pressure probably through the release of GABA and glutamate, respectively. The inhibitory action on blood pressure involves the stimulation of spinal GABA(A) and GABA(B) receptors whereas the excitatory response to glutamate appears to be mediated through the activation of spinal AMPA/kainate receptors.

Animals↗
PubMed2001

Studies on inhibition of human platelet function by sodium nitroprusside. Kinetic evaluation of the effect on aggregation and cyclic nucleotide content.

In this study, we explored the ability of sodium nitroprusside to inhibit the aggregation of human platelets in platelet-rich plasma (PRP) and whole blood and its effects on intracellular levels of guanosine 3',5'-cyclic monophosphate (cGMP) and adenosine 3',5'-cyclic monophosphate (cAMP). The experiments investigated dose-dependent effects of nitroprusside starting from concentrations in the range of circulating levels achievable in vivo during drug administration in humans. Furthermore, we investigated the time-course of both antiaggregating action and the influence on cyclic nucleotide synthesis. Results showed that sodium nitroprusside inhibited the aggregation induced by adenosine 5-diphosphate (ADP) and collagen starting from concentration as low as 2 micromol/l. The IC(50) value for ADP-induced aggregation in PRP was 18.7+/-2.4 micromol/l. The inhibition of platelet aggregation showed a time-dependent behaviour and was not reversible within 90 min. The accumulation of intraplatelet cGMP in the presence of sodium nitroprusside exhibited a comparable time-course characterized by an early increase, a steady state and a late further increase. The time-course of cAMP synthesis was very similar to that of cGMP. Our data evidenced a long-lasting inhibition of platelet responses by sodium nitroprusside and excluded a desensitization of platelet guanylyl cyclase after 3-h exposure to nitric oxide (NO). Furthermore, they indicated a role of cAMP accumulation in the antiaggregating effects of nitroso donor: the simultaneous increase of intracellular content of cAMP and cGMP can synergize in the reduction of the platelet responses.

Adenosine Diphosphate↗
PubMed1983

Comparative effects of nitroglycerin and nitroprusside on prostacyclin generation in adult human vessel wall.

The precise mechanism of vasodilatory actions of nitroso-compounds is not clear. It has been suggested that these drugs might modulate release of the vasodilator, prostacyclin, from cultured endothelial cells and bovine arteries or potentiate actions of prostacyclin. This study was designed to examine the effects of nitroglycerin and nitroprusside on prostacyclin release from adult human vasculature. Saphenous vein ring preparations were incubated with nitroglycerin or nitroprusside and arachidonic acid, the substrate for prostacyclin. Vascular rings incubated with nitroglycerin released significantly more prostacyclin (measured as 6-keto-prostaglandin F1 alpha, a stable hydrolysis product of prostacyclin by radioimmunoassay) compared with the control vascular rings (p less than 0.02). This increase was observed at the therapeutic concentrations of nitroglycerin (5 to 10 ng/ml). However, incubation of saphenous vein rings with nitroprusside in concentrations as high as 1 microgram/ml was not associated with any increase in prostacyclin release. Prior incubation of vascular rings with the cyclooxygenase blocker, indomethacin, inhibited nitroglycerin-induced prostacyclin release. Incubation of vascular rings with the selective thromboxane A2 blocker, OKY 1581, resulted in additional prostacyclin release with nitroglycerin treatment, presumably by inhibiting vessel wall-generated thromboxane A2. Nitroprusside had no significant effect on prostacyclin release from indomethacin-treated or OKY 1581-treated vascular rings. This study suggests significant stimulatory effects of nitroglycerin, but not of nitroprusside, on prostacyclin release from human saphenous vein. Nitroglycerin-induced prostacyclin release may be an important mechanism of its antiischemic actions in human subjects.

6-Ketoprostaglandin F1 alpha↗
PubMed2001

Nicardipine versus nitroprusside for breakthrough hypertension following carotid endarterectomy.

STUDY OBJECTIVE: To evaluate the effectiveness of nicardipine and nitroprusside for breakthrough hypertension following carotid endarterectomy. DESIGN: Prospective, randomized, double-blind, controlled effectiveness trial. SETTING: University-based surgical intensive care unit. PATIENTS: 60 ASA physical status I, II, III, and IV patients experiencing breakthrough hypertension at the time of admission to the intensive care unit (ICU). INTERVENTIONS: Patients received either nicardipine (n = 29) and placebo or nitroprusside (n = 31) and placebo for up to 6 hours postoperatively. Loading doses of nicardipine were provided, but placebo was used as a load for patients randomized to nitroprusside. MEASUREMENTS AND MAIN RESULTS: Rapidity and variability of blood pressure (BP) control were assessed. During the first 10 minutes, 83% of nicardipine patients compared to 23% of nitroprusside-treated patients, achieved BP control (p < 0.01). Following initial control, 12 nicardipine- and 24 nitroprusside-treated patients required additional titration of their infusions to maintain blood pressure within the targeted range (p < 0.05). No patient suffered a stroke, myocardial infarction, or was returned to the operating room (OR) for bleeding. CONCLUSIONS: Nicardipine administration produced more rapid BP control, most likely related to the administration of a loading dose. In addition to more rapid control, nicardipine-treated patients had less variability in BP and required significantly fewer additional interventions. Although no patient suffered a major event during this study, this study was not powered sufficiently to assess safety.

Aged↗
PubMed1999

Role of nitric oxide in isoprenaline and sodium nitroprusside-induced relaxation in human hand veins.

AIMS: Recent reports, largely in animal models, have suggested that either inhibition of nitric oxide (NO) synthase or endothelium removal in arteries inhibits the response to isoprenaline, a beta-adrenoceptor agonist, and also enhances the response to sodium nitroprusside, a nitrovasodilator. This in vivo study was designed to determine whether N(G)-monomethyl-L-arginine (L-NMMA), an inhibitor of NO synthesis, influences relaxation of human hand veins mediated by isoprenaline or by sodium nitroprusside. METHODS: Using the dorsal hand vein technique, full dose-response curves to bradykinin (0.27-278 ng min(-1), n=6), isoprenaline (2.12-271 ngmin(-1), n=8) and sodium nitroprusside (0.01-634 ng min(-1) n=7) were generated on separate occasions before and after L-NMMA co-infusion (50 microg min(-1)). RESULTS: In veins preconstricted with the alpha1-adrenoceptor-selective agonist phenylephrine, the three vasodilators induced maximal responses (Emax) of 119+/-35, 72+/-18 and 103+/-17%, respectively. L-NMMA inhibited relaxation to bradykinin by 64% (P=0.014) but did not influence relaxation induced by isoprenaline. The sensitivity to sodium nitroprusside was significantly enhanced by L-NMMA co-infusion (concentration shift of 2.3, P=0.031). CONCLUSIONS; We conclude that in human veins, spontaneously released NO does not play a major role in isoprenaline-induced relaxation. Our results also suggest that the effects of sodium nitroprusside in this vascular bed may be attenuated by endothelium-derived NO.

Adult↗
PubMedDate not supplied

Sodium nitroprusside-induced deliberate hypotension to facilitate patent ductus arteriosus ligation in dogs.

OBJECTIVE: To report the use of sodium nitroprusside to induce deliberate hypotension to reduce hemorrhage and facilitate surgical ligation of complicated patent ductus arteriosus (PDA) in dogs. STUDY DESIGN: Retrospective study. ANIMALS: Six dogs. METHODS: Hemorrhage occurred during surgical ligation of PDA in 5 dogs. Surgical dissection and isolation of the PDA were very difficult in a sixth dog that was considered to be at increased risk for ductus rupture. Sodium nitroprusside (5 to 25 microg/kg/min intravenously) was administered to these 6 dogs to induce hypotension to reduce blood loss and facilitate surgical ligation of the PDA. RESULTS: Sodium nitroprusside infusion reduced blood pressure (mean arterial pressure, 45 to 60 mm Hg) within 5 to 10 minutes and hemorrhage from the PDA, facilitating its surgical ligation. Recovery from surgery and anesthesia was uneventful in all 6 dogs. CONCLUSIONS: Sodium nitroprusside infusion can be used to induce deliberate hypotension in dogs to facilitate surgical ligation of PDA. CLINICAL RELEVANCE: Sodium nitroprusside infusion produces hypotension within 5 to 10 minutes and is easy to control, rapidly abates, and should help to facilitate surgical ligation of PDA.

Animals↗
PubMed1979

Rebound hemodynamic events after the abrupt withdrawal of nitroprusside in patients with severe chronic heart failure.

We studied the hemodynamic events that followed abrupt withdrawal of nitroprusside in 20 patients with severe chronic heart failure. With nitroprusside, cardiac index increased from 1.96 to 2.87 liters per minute per square meter of body-surface area, but it decreased to 1.66 (P less than 0.001) after withdrawal of nitroprusside. Left ventricular filling pressure and systemic vascular resistance decreased from 23.9 to 15.3 mm Hg and from 1642 to 921 dyn.sec.cm-5, respectively, with nitroprusside, but increased to 30.4 mm Hg and 2109 dyn.sec.cm-5 (both P less than 0.001) upon its discontinuation. These rebound changes were maximal 10 to 30 minutes after nitroprusside withdrawal and returned to control levels one to three hours later. Although in 17 of 20 patients, these rebound changes caused no or minimal exacerbation of symptoms, pulmonary edema, which resolved in three patients. Activation of reflex vasoconstrictive forces during vasodilator therapy may explain these effects of withdrawal.

Adult↗
PubMed1982

Effect of short-term infusion of sodium nitroprusside on mortality rate in acute myocardial infarction complicated by left ventricular failure: results of a Veterans Administration cooperative study.

Eight hundred twelve men with presumed acute myocardial infarction and left ventricular filling pressure of at least 12 mm Hg participated in a randomized double-blind placebo-controlled trial to assess the efficacy of a 48-hour infusion of sodium nitroprusside. The mortality rates at 21 days (10.4 per cent in the placebo group and 11.5 per cent in the nitroprusside group) and at 13 weeks (19.0 per cent and 17.0 per cent, respectively) were not significantly affected by treatment. The efficacy of nitroprusside was related to the time of treatment: the drug had a deleterious effect in patients whose infusions were started within nine hours of the onset of pain (mortality at 13 weeks, 24.2 per cent vs. 12.7 per cent; P = 0.025) and a beneficial effect in those whose infusions were begun later (mortality at 13 weeks, 14.4 per cent vs. 22.3 per cent; P = 0.04). Nitroprusside should probably not be used routinely in patients with high left ventricular filling pressures after acute myocardial infarction. However, the results in the patients given late treatment suggest that those with persistent pump failure might receive sustained benefit from short-term nitroprusside therapy.

Aged↗
PubMed2004

Nitroprusside increases gene transfer associated with intracoronary delivery of adenovirus.

Efficient gene transfer by vectors that can be easily delivered to target organs is desirable in clinical gene therapy. We tested the hypothesis that intracoronary infusion of the nitric oxide donor nitroprusside would increase the efficiency of adenovirus vector-mediated gene transfer to the heart. Intracoronary delivery of an adenovirus encoding murine adenylyl cyclase type VI (Ad.AC(VI)) was performed in adult pigs with and without simultaneous intracoronary infusion of nitroprusside. Animals were killed 12-14 days after Ad.AC(VI) delivery and myocardial adenylyl cyclase activity was measured. Addition of nitroprusside during intracoronary infusion of Ad.AC(VI) was associated with a 4-fold increase in cAMP-generating capacity in the left ventricle. Transgene expression was confirmed by immunoblotting. Intracoronary nitroprusside produced mild dose-dependent changes in blood pressure and heart rate during infusion. Intracoronary nitroprusside infusion is a safe and effective means to increase the extent of cardiac gene transfer with intracoronary delivery of adenovirus vectors.

Adenoviridae↗
PubMed1983

Effects of nitroprusside on myocardial blood flow in acute regional coronary ischaemia in conscious dogs with and without left ventricular distension.

To determine the effects of nitroprusside on regional myocardial ischaemia, experiments were done in 11 conscious dogs with balloon-cuff occluders implanted around the left anterior descending coronary artery (LAD). Regional myocardial blood flow by the microsphere method was determined during 5 min periods of temporary LAD occlusion with and without nitroprusside infusion. Nitroprusside decreased aortic mean and left ventricular diastolic pressures. Blood flow increased to ischaemic myocardium supplied by the occluded LAD and to non-ischaemic myocardium supplied by the patent left circumflex coronary artery. Experiments were repeated on a separate day in the presence of left ventricular distension in the same dogs. Nitroprusside again decreased aortic mean and left ventricular diastolic pressures and increased the blood flow to both ischaemic and non-ischaemic myocardial regions. These results suggest that nitroprusside can improve perfusion to acutely ischaemic myocardial tissue despite a fall in aortic pressure, presumably by decreasing resistance to flow in coronary collateral vessels or by decreasing the myocardial tissue pressure.

Animals↗
PubMed1994

Assessment of ability of levcromakalim and sodium nitroprusside to reverse the cardiovascular effects of nitric oxide synthase inhibition in the anaesthetised pig.

OBJECTIVE: The aim was to test the ability of levcromakalim, a potassium channel opener, and sodium nitroprusside, a nitric oxide donor, to reverse the systemic and pulmonary vasoconstrictor actions of NG-nitro-L-arginine methyl ester (L-NAME), and thus to restore cardiac output in anaesthetised pigs. METHODS: In separate groups of pigs administration of a bolus of L-NAME (10 mg.kg-1) was followed either by no further agent (control group; n = 8) or by increasing bolus doses of levcromakalim (10, 20, and 40 micrograms.kg-1; n = 8) or by increasing infused doses of sodium nitroprusside (1, 2, and 4 micrograms.kg-1.min-1 for 15 min at each dose). The same doses of levcromakalim and sodium nitroprusside were also given to pigs (n = 6 in each group) which had been pretreated with saline rather than L-NAME. The changes in systemic and pulmonary haemodynamic indices and cardiac output as a result of each intervention were measured at each stage and compared between and within drug groups. RESULTS: In each group, the bolus of L-NAME caused increases in systemic vascular resistance, mean arterial pressure, pulmonary vascular resistance, and mean pulmonary artery pressure, and a reduction in cardiac output. These effects were significantly different from pretreatment values at 15 min, and were maintained for at least 60 min when no further agent was given. The subsequent administration of levcromakalim caused significant reductions in systemic vascular resistance and mean arterial pressure, the effects being greater than in animals that had been pretreated with saline rather than L-NAME. Pulmonary vascular resistance and mean pulmonary artery pressure were also reduced, but to a lesser degree. Cardiac output was partially but significantly restored. The subsequent administration of sodium nitroprusside caused significant reductions in systemic vascular resistance, mean arterial pressure, pulmonary vascular resistance, and mean pulmonary artery pressure. These effects were significantly greater than those in animals that had been pretreated with saline rather than L-NAME. Cardiac output was weakly, though significantly restored. CONCLUSIONS: Increased systemic vascular resistance following a bolus of L-NAME (10 mg.kg-1) is reversed by subsequent administration of levcromakalim (10-40 micrograms.kg-1) or sodium nitroprusside (1-4 micrograms.kg-1.min-1) associated with partial restoration of cardiac output. The degree to which cardiac output is restored by these two agents is limited by a concomitant reduction in preload.

Amino Acid Oxidoreductases↗
PubMed2004

Intracervical sodium nitroprusside versus vaginal misoprostol in first trimester surgical termination of pregnancy: a randomized double-blinded controlled trial.

BACKGROUND: Results from small-scale randomized studies on the effectiveness of different preparations of nitric oxide donors in cervical priming before first trimester termination of pregnancies are not consistent. We compared sodium nitroprusside gel to misoprostol, the standard agent for cervical priming in this randomized double-blinded controlled trial. METHODS: Two hundred pregnant patients between 8 to 12 weeks admitted for surgical termination of pregnancy were recruited. They were randomized into either 400 microg vaginal misoprostol and intracervical placebo gel, or 10 mg intracervical sodium nitroprusside gel and placebo tablets 3 h before the procedure. The baseline cervical dilatation and cumulative force required to dilate the cervix from 4 to 9 mm were measured with a tonometer. Blood pressure was measured and side effects were assessed. RESULTS: The cumulative force to dilate the cervix from 4 to 9 mm was significantly higher in the sodium nitroprusside group, and the difference remained when a sub-group analysis was performed according to parity. Baseline cervical dilatation, duration of operation and operative blood loss were all in favour of misoprostol. Transient drop in blood pressure was observed after sodium nitroprusside treatment. CONCLUSIONS: Intracervical sodium nitroprusside is not as effective as misoprostol in cervical priming.

Abortifacient Agents, Nonsteroidal↗
PubMed1999

Effects of sodium nitroprusside and phenylephrine on blood flow in free musculocutaneous flaps during general anesthesia.

BACKGROUND: Hypoperfusion and necrosis in free flaps used to correct tissue defects remain important clinical problems. The authors studied the effects of two vasoactive drugs, sodium nitroprusside and phenylephrine, which are used frequently in anesthetic practice, on total blood flow and microcirculatory flow in free musculocutaneous flaps during general anesthesia. METHODS: In a porcine model (n = 9) in which clinical conditions for anesthesia and microvascular surgery were simulated, latissimus dorsi free flaps were transferred to the lower extremity. Total blood flow in the flaps was measured using ultrasound flowmetry and microcirculatory flow was measured using laser Doppler flowmetry. The effects of sodium nitroprusside and phenylephrine were studied during local infusion through the feeding artery of the flap and during systemic administration. RESULTS: Systemic sodium nitroprusside caused a 30% decrease in mean arterial pressure, but cardiac output did not change. The total flow in the flap decreased by 40% (P < 0.01), and microcirculatory flow decreased by 23% in the skin (P < 0.01) and by 30% in the muscle (P < 0.01) of the flap. Sodium nitroprusside infused locally into the flap artery increased the total flap flow by 20% (P < 0.01). Systemic phenylephrine caused a 30% increase in mean arterial pressure, whereas heart rate, cardiac output, and flap blood flow did not change. Local phenylephrine caused a 30% decrease (P < 0.01) in the total flap flow. CONCLUSIONS: Systemic phenylephrine in a dose increasing the systemic vascular resistance and arterial pressure by 30% appears to have no adverse effects on blood flow in free musculocutaneous flaps. Sodium nitroprusside, however, in a dose causing a 30% decrease in systemic vascular resistance and arterial pressure, causes a severe reduction in free flap blood flow despite maintaining cardiac output.

Anesthesia, General↗
PubMed1993

Use of vitamin B12 in the treatment and prevention of nitroprusside-induced cyanide toxicity.

OBJECTIVE: To review the mechanism of action, safety, and efficacy of hydroxocobalamin in the treatment and prevention of nitroprusside-induced cyanide toxicity. DATA SOURCES: English and foreign-language journal articles and reference texts identified from Index Medicus. Both animal and human studies were included. DATA SYNTHESIS: High-dose or prolonged therapy with nitroprusside in patients with hepatic or renal dysfunction increases the risk for nitroprusside-induced cyanide or thiocyanate toxicity, respectively. Hydroxocobalamin has been shown to significantly reduce RBC and plasma cyanide concentrations in animals and surgical patients without producing clinically important adverse effects or toxic metabolites. Thiosulfate infusions also decrease cyanide toxicity but can cause accumulation of thiocyanate resulting in clinical toxicity. Cyanocobalamin cannot effectively remove cyanide due to poor binding. CONCLUSIONS: Hydroxocobalamin is a safe and effective agent in the prevention and treatment of nitroprusside-induced cyanide toxicity. Prolonged or high-dose infusions of nitroprusside should be minimized in critically ill patients, especially if hepatic and/or renal dysfunction is present.

Animals↗
PubMed1999

Flow dependence of forearm noradrenaline overflow, as assessed during mental stress and sodium nitroprusside infusion.

OBJECTIVE: To evaluate the influence of blood flow on measurements of regional sympathetic nerve activity by radiotracer methodology ([3H]noradrenaline). DESIGN: Ten healthy men were studied under two conditions of elevated forearm blood flow: mental stress (Stroop colour word conflict test) and an intra-arterial infusion of sodium nitroprusside. METHODS: Arterial blood pressure was measured invasively and forearm blood flow with strain-gauge plethysmography. Arterial and venous plasma adrenaline and noradrenaline were measured with high-performance liquid chromatography, and regional and total noradrenaline spillover were calculated. RESULTS: During mental stress, mean arterial pressure increased by 17%, heart rate by 16 beats/min, forearm blood flow by 117%, while forearm vascular resistance decreased by 44% (P < 0.001 for all). Sodium nitroprusside increased forearm blood flow dose-dependently, but elicited only minor effects on systemic haemodynamics. Mental stress increased arterial plasma noradrenaline by 52% (P < 0.001), and total body noradrenaline spillover by 75% (P < 0.001). During sodium nitroprusside infusion, arterial plasma noradrenaline increased only slightly and total body noradrenaline spillover was unaffected Forearm noradrenaline overflow increased from 5.4 +/- 0.9 to 16.9 +/- 2.6 pmol/min per I (P < 0.001) during mental stress and from 6.6 +/- 0.8 to 16.9 +/- 3.7 pmol/min per I (P < 0.001) during the second dose-step of sodium nitroprusside infusion. By intra-individual comparisons of forearm noradrenaline overflow increases during mental stress and during sodium nitroprusside infusion, with similar forearm blood flow increases, the flow dependence of forearm noradrenaline overflow was estimated. During mental stress, about 60% (median value, range 29-112%) of the increase in forearm noradrenaline overflow was attributed to the increase in forearm blood flow, whereas 40% was considered to reflect increased sympathetic nerve activity. CONCLUSIONS: There seems to be a considerable flow dependence of the regional overflow of noradrenaline, that is, a component of simple wash-out of noradrenaline from the forearm tissues during vasodilation. However, the present results still indicate that sympathetic nerve activity in the forearm is increased during mental stress, justifying the radiotracer technique for semiquantitative measurements, also during vasodilation.

Adult↗
PubMed1980

Hypotensive effects of N,N-din-n-propylodopamine in the anesthetized dog: comparison with sodium nitroprusside.

N,N-Din-n-propyldopamine (DPDA), a dopamine (DA) vascular agonist without beta 1-adrenergic activity, was compared with mitroprusside in pentobarbital-anesthetized dogs. DPDA was infused intravenously at 20, 40, and 80 microgram/kg/min. DPDA caused dose-related reductions in mean arterial pressure when infused at 20 and 40 microgram/kg/min; no further decrease occurred at 80 microgram/kg/min. Sodium nitroprusside, 1-6 microgram/kg/min, approximately equaled the hypotension produced by 40 microgram/kg/min of DPDA. DPDA differed from sodium nitroprusside in causing a more rapid fall in mean arterial pressure and a more rapid recovery upon discontinuation. DPDA had no effect on pulmonary arterial pressure, but sodium nitroprusside reduced it. DPDA reduced heart rate; sodium nitroprusside increased heart rate. Hexamethonium. 10 mg/kg, significantly reduced the hypotension produced by DPDA. The DA antagonist, sulpiride, completely eliminated the reduction in blood pressure caused by DPDA. Neither hexamethonium nor sulpiride affected the hypotension produced by sodium nitroprusside. These studies suggest that DPDA reduces blood pressure in part by inhibiting the sympathetic nervous system and in part by vasodilation secondary to action on DA vascular receptors.

Animals↗
PubMedDate not supplied

The renal response to diltiazem and nifedipine: comparison with nitroprusside.

We undertook a systematic comparison of the effects of diltiazem and nifedipine and a nonspecific vasodilator, sodium nitroprusside, on renal perfusion, function, and activation of potentially relevant neurohormonal systems in the anesthetized dog. These agents were employed to reduce blood pressure to two levels, a mean arterial pressure level of 100-110 mm Hg, and a subtherapeutic level of 75-85 mm Hg. Renal plasma flow (ERPF) and glomerular filtration rate (GFR) were estimated as the clearances of p-aminohippurate and inulin, respectively. All studies with vasodilators were compared with a group which received placebo over an identical time period. The agents differed both in their action on the renal blood supply and in their activation of the renin-angiotensin-aldosterone and sympathetic nervous systems. ERPF was better maintained at both blood pressure levels with nitroprusside than with either diltiazem (p less than 0.005) or nifedipine (p less than 0.005). GFR was better maintained with nitroprusside and diltiazem than with nifedipine. The rise in plasma catecholamines and plasma renin activity was greatest with nifedipine, least with nitroprusside, and intermediate with diltiazem. Diltiazem was also associated with substantially less stimulation of aldosterone release than was nifedipine. Diltiazem and nifedipine are known to have greater renal vasodilator action when infused into the renal artery than nitroprusside. The better-sustained renal plasma flow and glomerular filtration rate during systemic administration with the latter may well reflect the role of calcium in renal autoregulation and the angiotensin-renin feedback loop. Despite an apparent shared mechanism of action, the calcium-entry-blocking agents differ sufficiently that therapeutic implications are possible.

Animals↗