Hypotensive and antihypertensive effects of an aqueous extract from Guinep fruit (Melicoccus bijugatus Jacq) in rats

Abstract Melicoccus bijugatus Jacq (Mb) has been reported to have cardiovascular modulatory effects. In this study, we evaluated the antihypertensive effects and mechanism of action of Mb on NG-Nitro-l-arginine Methyl Ester (l-NAME) and Deoxycorticosterone Acetate (DOCA) rat models. Aqueous extract of Mb fruit (100 mg/kg) was administered for 6 weeks to rats by gavage and blood pressure was recorded. Effects of the extract on vascular reactivity was evaluated using isolated organ baths, and tissues were collected for biochemical and histological analysis. The systolic blood pressure (SBP), diastolic blood pressure (DBP) and mean arterial pressure (MAP) were significantly (P < 0.05) reduced with extract (100 mg/kg) administration and treatment compared to the hypertensive models. Mb (100 µg/mL) reduced the vascular contractility induced by phenylephrine (PE), and caused a dose-dependent relaxation of PE-induced contraction of aortic vascular rings. The vasorelaxation properties seemed to be endothelium dependent, as well as nitric oxide (NO) and guanylyl cyclase, but not prostaglandin dependent. Histomicrograph of transverse sections of the ventricles from the Mb group did not show abnormalities. The extract significantly (P < 0.05) reduced an l-NAME induced elevation of cardiac output and Creatine Kinase Muscle-Brain (CKMB), but had no significant impact on the activities of arylamine N-acetyltransferase. In conclusion, Mb significantly decreased blood pressure in hypertensive models. The extract possesses the ability to induce endothelium dependent vasodilation, which is dependent on guanylyl cyclase but not prostaglandins.

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Effects of NG-nitro-L-arginine methyl ester on renal function and blood pressure

AJP Renal Physiology ◽

10.1152/ajprenal.1991.261.6.f1033 ◽

1991 ◽

Vol 261 (6) ◽

pp. F1033-F1037 ◽

Cited By ~ 42

Author(s):

V. Lahera ◽

M. G. Salom ◽

F. Miranda-Guardiola ◽

S. Moncada ◽

J. C. Romero

Keyword(s):

Nitric Oxide ◽

Blood Pressure ◽

Renal Function ◽

Methyl Ester ◽

Renal Plasma Flow ◽

Urinary Sodium Excretion ◽

Systemic Blood Pressure ◽

Synthesis Inhibitor ◽

Renal Changes ◽

Dose Dependent

The dose-dependent effects of intravenous infusions of nitric oxide (NO) synthesis inhibitor, NG-nitro-L-arginine methyl ester (L-NAME; 0.1, 1, 10, and 50 micrograms.kg-1.min-1), were studied in anesthetized rats to determine whether the inhibitory actions of L-NAME are manifested primarily in alterations of renal function or whether they are the consequences of the increase in systemic blood pressure. Mean arterial pressure (MAP) was not altered by the intravenous L-NAME infusions of 0.1 and 1.0 microgram.kg-1.min-1. However, 0.1 microgram.kg-1.min-1 L-NAME induced a 30% decrease in urine flow rate (UV). The administration of 1.0 microgram.kg-1.min-1 L-NAME, in addition to decreasing UV, also decreased urinary sodium excretion (UNaV) and renal plasma flow (RPF). The intravenous L-NAME infusions of 10.0 and 50.0 microgram.kg-1.min-1 intravenous L-NAME infusions of 10.0 and 50.0 microgram.kg-1.min-1 produced significant increases in MAP that reversed the initial fall in UV and UNaV, despite decreasing RPF and glomerular filtration rate (GFR). The administration of L-arginine alone (10 micrograms.kg-1.min-1) did not modify any of the parameters measured, but it effectively prevented all the hemodynamic and renal changes induced by the infusion of 50 micrograms.kg-1.min-1 L-NAME. These results suggest that the decrease in nitric oxide production induced by the intravenous infusion of L-NAME affects renal excretion of sodium and water in the absence of any significant change in blood pressure. At larger doses, L-NAME also produces hypertension that overrides the initial antinatriuretic effect.

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Effect of magnesium supplementation on blood pressure and vascular reactivity in nitric oxide synthase inhibition-induced hypertension model

Clinical and Experimental Hypertension ◽

10.3109/10641963.2015.1036063 ◽

2015 ◽

Vol 37 (8) ◽

pp. 633-642 ◽

Cited By ~ 5

Author(s):

Filiz Basralı ◽

Günnur Koçer ◽

Pınar Ülker Karadamar ◽

Seher Nasırcılar Ülker ◽

Leyla Satı ◽

...

Keyword(s):

Nitric Oxide ◽

Blood Pressure ◽

Nitric Oxide Synthase ◽

Vascular Reactivity ◽

Magnesium Supplementation ◽

Induced Hypertension ◽

Oxide Synthase

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Effects of corn silk aqueous extract on intraocular pressure of ocular hypertensive human subjects

African Vision and Eye Health ◽

10.4102/aveh.v72i3.282 ◽

2013 ◽

Vol 72 (3) ◽

Author(s):

G.O. George ◽

F.K. Idu ◽

L.F.O. Obika

Keyword(s):

Blood Pressure ◽

Body Weight ◽

Intraocular Pressure ◽

Aqueous Extract ◽

Zea Mays L ◽

Human Subjects ◽

Hypotensive Effect ◽

Peak Effect ◽

Corn Silk ◽

Dose Dependent

Stigma/style of Zea mays L (Corn silk) has been documented to have hypotensive effect on blood pressure and to relieve oedema. However we are not aware of any literature on its hypotensive effect on intraocular pressure (IOP) of humans or animals. We studied the effects of water only, masked doses of corn silk aqueous extract (60 mg/kg, 130 mg/kg, 192.5 mg/kg and 260 mg/kg body weight) on the IOP and blood pressure (BP) of twenty normotensives and twenty ocular hypertensive subjects. Also we compared the effects of the varied doses of corn silk aqueous extract (CSAE) with masked doses (5 mg/kg and 10 mg/kg body weight) of acetazolamide on IOP of ocular hypertensive subjects only. The results showed that the last three doses of CSAE lowered IOP and BP significantly (p<0.001) within eight hours of administration. The peak effect on IOP was observed after four hours while the peak effect on BP was observed after three hours of administration in the normotensives and ocular hypertensive subjects likewise the hypotensive effect was dose-dependent. The results also showed that 130 mg/kg body weight of CSAE produced the same hypotensive effect on IOP of ocular hypertensive subjects as 5 mg/kg body weight of acetazolamide. Therefore CSAE may have some IOP lowering effects that require further investigation in the management of ocular hypertension. (S Afr Optom 2013 72(3) 133-143)

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The effect of chronic nitric oxide inhibition on vascular reactivity and blood pressure in pregnant rats

Sao Paulo Medical Journal ◽

10.1590/s1516-31801999000500004 ◽

1999 ◽

Vol 117 (5) ◽

pp. 197-204 ◽

Cited By ~ 7

Author(s):

Nilton Hideto Takiuti ◽

Maria Helena Cetelli Carvalho ◽

Soubhi Kahhale ◽

Dorothy Nigro ◽

Hermes Vieira Barbeiro ◽

...

Keyword(s):

Nitric Oxide ◽

Blood Pressure ◽

Vascular Reactivity ◽

Unit Weight ◽

Control Group ◽

Pregnant Rats ◽

Nitric Oxide Inhibition ◽

Female Wistar Rats ◽

Main Component ◽

Oxide Inhibition

CONTEXT: The exact mechanism involved in changes in blood pressure and peripheral vascular resistance during pregnancy is unknown. OBJECTIVE:To evaluate the importance of endothelium-derivated relaxing factor (EDRF) and its main component, nitric oxide, in blood pressure and vascular reactivity in pregnant rats. DESIGN: Clinical trial in experimentation animals. SETTING: University laboratory of Pharmacology. SAMPLE: Female Wistar rats with normal blood pressure, weight (152 to 227 grams) and age (90 to 116 days). INTERVENTION: The rats were divided in to four groups: pregnant rats treated with L-NAME (13 rats); pregnant control rats (8 rats); virgin rats treated with L-NAME (10 rats); virgin control rats (12 rats). The vascular preparations and caudal blood pressure were obtained at the end of pregnancy, or after the administration of L-NAME in virgin rats. MAIN MEASUREMENTS: The caudal blood pressure and the vascular response to acetylcholine in pre-contracted aortic rings, both with and without endothelium, and the effect of nitric oxide inhibition, Nw-L-nitro-arginine methyl-ester (L-NAME), in pregnant and virgin rats. The L-NAME was administered in the drinking water over a 10-day period. RESULTS: The blood pressure decreased in pregnancy. Aortic rings of pregnant rats were more sensitive to acetylcholine than those of virgin rats. After L-NAME treatment, the blood pressure increased and relaxation was blocked in both groups. The fetal-placental unit weight of the L-NAME group was lower than that of the control group. CONCLUSION: Acetylcholine-induced vasorelaxation sensitivity was greater in pregnant rats and that blood pressure increased after L-NAME administration while the acetylcholine-induced vasorelaxation response was blocked.

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Effects of obesity on endothelium-dependent reactivity during acute nitric oxide synthase inhibition: modulatory role of endothelin

Clinical Science ◽

10.1042/cs103s013s ◽

2002 ◽

Vol 103 (s2002) ◽

pp. 13S-15S ◽

Cited By ~ 29

Author(s):

Tobias TRAUPE ◽

Livius V. D'USCIO ◽

Klaus MUENTER ◽

Henning MORAWIETZ ◽

Wilhelm VETTER ◽

...

Keyword(s):

Nitric Oxide ◽

Nitric Oxide Synthase ◽

Carotid Artery ◽

Vascular Reactivity ◽

Receptor Blockade ◽

Obese Mice ◽

Vascular Rings ◽

Eta Receptor ◽

Eta Receptor Antagonist ◽

Oxide Synthase

This study investigated vascular reactivity in response to acetylcholine, in the presence of acute inhibition of nitric oxide synthase, in the carotid artery and aorta of obese C57Bl6/J mice fed on a high-fat diet for 30 weeks, and of control mice. A subgroup of obese animals was also treated with the ETA receptor antagonist darusentan (50mg·kg-1·day-1). In vascular rings from control animals, acetylcholine caused endothelium-dependent contractions in the carotid artery, but not in the aorta. In vascular rings from obese mice, contractility to acetylcholine was also evident in the aorta, and that in the carotid artery was increased compared with control mice. ETA receptor blockade by darusentan treatment of the obese mice prevented enhanced vasoconstriction to acetylcholine, resulting in mild vasodilatation. Thus obesity increases endothelium-dependent vasoconstriction in the absence of endothelial nitric oxide. This effect can be completely prevented by chronic ETA receptor blockade, suggesting that endothelin modulates increased endothelium-dependent vasoconstriction in obesity.

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Effects of Vasopressin in Septic Shock

AACN Advanced Critical Care ◽

10.4037/15597768-2008-3006 ◽

2008 ◽

Vol 19 (3) ◽

pp. 281-287

Author(s):

Margaret S. Ruggiero

Keyword(s):

Nitric Oxide ◽

Blood Pressure ◽

Septic Shock ◽

Cardiovascular Effects ◽

The Body ◽

Myocardial Depression ◽

Restore Blood Pressure ◽

Dose Dependent ◽

Pituitary Adrenal Axis ◽

Major Mediator

Septic shock continues to be one of the leading causes of death in the intensive care unit today. The confluence of many factors contributes to the deterioration of patients’ condition in septic shock. Increased levels of nitric oxide, in part, mediate the cardiovascular effects of septic shock. Nitric oxide is major mediator of vasodilation and hypotension as well as myocardial depression. It also contributes to decreased production and release of endogenous vasopressin. Vasopressin effects are actualized by stimulation of V1, V2, and V3 receptors located in various parts of the body. The response is dose dependent. Endogenous vasopressin and angiotensin II act synergistically to preserve and restore blood pressure levels. Decreased circulating vasopressin contributes to adrenal insufficiency via hypothalamic-pituitary-adrenal axis suppression and increased catecholamine resistance to vasopressors. Exogenous vasopressin supplementation in physiologic doses has been shown to improve blood pressure levels and decrease vasopressor needs in patients with septic shock.

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Cardiovascular actions of trout urotensin II in the conscious trout, Oncorhynchus mykiss

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1996.271.5.r1335 ◽

1996 ◽

Vol 271 (5) ◽

pp. R1335-R1343 ◽

Cited By ~ 8

Author(s):

J. C. Le Mevel ◽

K. R. Olson ◽

D. Conklin ◽

D. Waugh ◽

D. D. Smith ◽

...

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Arterial Blood Pressure ◽

Cardiovascular Effects ◽

Pressor Effect ◽

Urotensin Ii ◽

Cardinal Vein ◽

Vascular Rings ◽

Arterial Blood ◽

Dose Dependent

The central and peripheral cardiovascular effects of synthetic trout urotensin II (UII) were investigated in the conscious rainbow trout. Intracerebroventricular injection of 50 pmol UII produced a slight (3%) but significant (P < 0.05) increase in heart rate but had no effect on mean arterial blood pressure. Injection of 500 pmol UII icv produced a significant (P < 0.05) rise (8%) in blood pressure with no change in heart rate. In contrast to the weak pressor effect of centrally administered UII, intra-arterial injection of UII produced a dose-dependent increase in arterial blood pressure and decrease in heart rate with significant (P < 0.05) effects on both parameters observed at a dose of 25 pmol. Higher doses of the peptide produced a sustained decrease in cardiac output that accompanied the bradycardia and rise in arterial blood pressure. The UII-induced bradycardia, but not the increase in pressure, was abolished by pretreatment with phentolamine. Trout UII produced a sustained and dose-dependent contraction of isolated vascular rings prepared from trout efferent branchial [-log 50% of the concentration producing maximal contraction (pD2) = 8.30] and celiacomesenteric (pD2 = 8.22) arteries but was without effects on vascular rings from the anterior cardinal vein. The data indicate that the pressor effect of UII in trout is mediated predominantly, if not exclusively, by an increase in systemic vascular resistance. The UII-induced hypertensive response does not seem to involve release of catecholamines, but the bradycardia may arise from adrenergic-mediated activation of cardioinhibitory baroreflexes.

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