Hypotensive, cardiodepressant, and vasorelaxant activities of black currant (Ribes nigrum ‘Ben Sarek’) juice

2016 ◽  
Vol 94 (10) ◽  
pp. 1102-1105 ◽  
Author(s):  
Suzana Branković ◽  
Bojana Miladinović ◽  
Mirjana Radenković ◽  
Marija Gočmanac Ignjatović ◽  
Milica Kostić ◽  
...  

The aim of this study was to evaluate the effects of black currant (Ribes nigrum L. ‘Ben Sarek’) juice on the blood pressure and frequency of cardiac contractions, as well as vasomotor responses of rat aortic rings. Arterial blood pressure was measured directly from the carotid artery in the anaesthetized rabbits. The aortic rings were pre-contracted with KCl (80 mmol·L−1), after which black currant juice was added. An intravenous injection of black currant juice (0.33–166.5 mg·kg−1) induced a significant and dose-dependent decrease of rabbit arterial blood pressure and heart rate. The black currant juice decreased arterial blood pressure of rabbit by 22.33% ± 3.76% (p < 0.05) and heart rate by 17.18% ± 2.93% (p < 0.05). Cumulative addition of the black currant juice (0.01–3 mg·mL−1) inhibited concentration-dependent KCl induced contractions of the isolated rat aorta. The black currant juice, at the concentration of 3 mg·mL−1, caused a maximum relaxation of 21.75% ± 3.15% (p < 0.05). These results demonstrate that black currant juice can induce hypotension. The hypotensive effect of the black currant may occur as the consequence of its inhibitory activity on the rate of heart contraction and vasorelaxant effects.

1996 ◽  
Vol 271 (5) ◽  
pp. R1335-R1343 ◽  
Author(s):  
J. C. Le Mevel ◽  
K. R. Olson ◽  
D. Conklin ◽  
D. Waugh ◽  
D. D. Smith ◽  
...  

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.


Author(s):  
Cristina Del Seppia ◽  
Cristina Del Seppia ◽  
Giuseppe Federighi ◽  
Enza Fommei ◽  
Sergio Ghione ◽  
...  

Objectives: Previous research has shown that submaximal mouth opening by mandibular extension (ME) is followed by a prolonged reduction in blood pressure. This effect was observed in young and adult normotensive and hypertensive rats and in young normotensive human subjects. Methods: We assessed the effects of a ME for 10 minutes obtained with a fixed mouth opener in both hypertensive adult humans (aged 55 years or older) and elderly (6-7 months) anaesthetized, hypertensive rats (SHR). Blood pressure and heart rate were measured every 10 minutes by non-invasive automatic recorders for 30 minutes before and 120 minutes after the procedure. Nine human hypertensive subjects (7 experimental and 2 controls) and seven spontaneously hypertensive rats (5 experimental and 2 controls) were tested. Results: A statistically significant reduction in systolic blood pressure (SBP), mean arterial blood pressure (MABP) and heart rate (HR) was observed after ME in the seven hypertensive human subjects, in whom an average decrease of 15 mmHg for SBP, 10 mmHg for MABP and 7 bpm for HR, was observed. A similar hypotensive effect was recorded in spontaneously hypertensive rats that displayed a statistically significant decrease of SBP, DBP and MABP, amounting to about 40-50 mmHg. Conclusion: This study provides the first evidence that ME has an important and prolonged hypotensive effect when applied to subjects with high blood pressure, making their arterial blood pressure decrease toward normal values for at least two hours.


2014 ◽  
Vol 63 (6) ◽  
pp. 435-438 ◽  
Author(s):  
Kunihiko Tanaka ◽  
Shiori Tokumiya ◽  
Yumiko Ishihara ◽  
Yumiko Kohira ◽  
Tetsuro Katafuchi

1991 ◽  
Vol 81 (6) ◽  
pp. 727-732 ◽  
Author(s):  
Marohito Murakami ◽  
Hiromichi Suzuki ◽  
Atsuhiro Ichihara ◽  
Mareo Naitoh ◽  
Hidetomo Nakamoto ◽  
...  

1. The effects of l-arginine on systemic and renal haemodynamics were investigated in conscious dogs. l-Arginine was administered intravenously at doses of 15 and 75 μmol min−1 kg−1 for 20 min. 2. Mean arterial blood pressure, heart rate and cardiac output were not changed significantly by l-arginine infusion. However, l-arginine infusion induced a significant elevation of renal blood flow from 50 ± 3 to 94 ± 12 ml/min (means ± sem, P < 0.01). 3. Simultaneous infusion of NG-monomethyl-l-arginine (0.5 μmol min−1 kg−1) significantly inhibited the increase in renal blood flow produced by l-arginine (15 μmol min−1 kg−1) without significant changes in mean arterial blood pressure or heart rate. 4. Pretreatment with atropine completely inhibited the l-arginine-induced increase in renal blood flow, whereas pretreatment with indomethacin attenuated it (63 ± 4 versus 82 ± 10 ml/min, P < 0.05). 5. A continuous infusion of l-arginine increased renal blood flow in the intact kidney (55 ± 3 versus 85 ± 9 ml/min, P < 0.05), but not in the contralateral denervated kidney (58 ± 3 versus 56 ± 4 ml/min, P > 0.05). 6. These results suggest that intravenously administered l-arginine produces an elevation of renal blood flow, which may be mediated by facilitation of endogenous acetylcholine-induced release of endothelium-derived relaxing factor and vasodilatory prostaglandins.


1979 ◽  
Vol 237 (3) ◽  
pp. H381-H385 ◽  
Author(s):  
E. F. Ellis ◽  
E. P. Wei ◽  
H. A. Kontos

To determine the possible role that endogenously produced prostaglandins may play in the regulation of cerebral blood flow, the responses of cerebral precapillary vessels to prostaglandins (PG) D2, E2, G2, and I2 (8.1 X 10(-8) to 2.7 X 10(-5) M) were studied in cats equipped with cranial windows for direct observation of the microvasculature. Local application of PGs induced a dose-dependent dilation of large (greater than or equal to 100 microns) and small (less than 100 microns) arterioles with no effect on arterial blood pressure. The relative vasodilator potency was PGG2 greater than PGE2 greater than PGI2 greater than PGD2. With all PGs, except D2, the percent dilation of small arterioles was greater than the dilation of large arterioles. After application of prostaglandins in a concentration of 2.7 X 10(-5) M, the mean +/- standard error of the percent dilation of large and small arterioles was, respectively, 47.6 +/- 2.7 and 65.3 +/- 6.1 for G2, 34.1 +/- 2.0, and 53.6 +/- 5.5 for E2, 25.4 +/- 1.8, and 40.2 +/- 4.6 for I2, and 20.3 +/- 2.5 and 11.0 +/- 2.2 for D2. Because brain arterioles are strongly responsive to prostaglandins and the brain can synthesize prostaglandins from its large endogenous pool of prostaglandin precursor, prostaglandins may be important mediators of changes in cerebral blood flow under normal and abnormal conditions.


2020 ◽  
Author(s):  
Bharti Bhandari ◽  
Manisha Mavai ◽  
Yogendra Raj Singh ◽  
Bharati Mehta ◽  
Omlata Bhagat

A single episode of breath-holding (BH) is known to elevate the blood pressure, and regular breathing exercise lowers the blood pressure. This prompted us to investigate how a series of BH epochs would affect the cardiovascular system. To observe arterial blood pressure (ABP) and heart rate (HR) changes associated with a series of “BH epochs” following maximum inspiration and maximum expiration and find the underlying mechanisms for the change by autonomic activity. Thirty-five healthy young adults were instructed to hold their breath repetitively, for 5 minutes, in two patterns, one following maximum inspiration and other following maximum expiration. ABP and ECG (for Heart Rate Variability) were continuously recorded at rest and during both the maneuvers. Capillary blood gases (BG) were zanalyzed at baseline and at the breakpoint of the last epoch of BH. ABP rose significantly at the breakpoint during both the maneuvers. No change in HR was observed. There was significant fall in PO2 from 94.7 (4.1) mmHg at baseline to 79.1 (9.0) mmHg during inspiratory and 76.90 (12.1) mmHg during expiratory BH. Similarly, SPO2 decreased from 96.3 (1.9) % at baseline to 95.4 (1.5) % and 94.5 (2.7) % during inspiratory and expiratory BH, respectively. Rise in PCO2 from 39.5(3.1) mmHg at baseline to 42.9 (2.7) mmHg and 42.1 (2.8) mmHg during inspiratory and expiratory BH respectively was observed. There was no significant correlation between blood gases and arterial blood pressure. Among HRV parameters, a significant decrease in SDNN, RMSSD, HFnu, total power and SD1/SD2 and the significant increase in LFnu, LF/HF and SD2 were observed during both BH patterns. Rhythmic BH patterns affect the cardiovascular system in similar way as a single episode of BH. Sympathetic overactivity could be the postulated mechanism for the same. © 2019 Tehran University of Medical Sciences. All rights reserved. Acta Med Iran 2019;57(8):492-498.


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