scholarly journals Garlic Attenuates Plasma and Kidney ACE-1 and AngII Modulations in Early Streptozotocin-Induced Diabetic Rats: Renal Clearance and Blood Pressure Implications

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Khaled K. Al-Qattan ◽  
Martha Thomson ◽  
Divya Jayasree ◽  
Muslim Ali
Keyword(s):  
Blood Pressure ◽  
Renal Clearance ◽  
Renin Angiotensin System ◽  
Diabetic Rats ◽  
Converting Enzyme ◽  
Angiotensin I ◽  
Angiotensin System ◽  
Angiotensin I Converting Enzyme ◽  
Type 1 Dm

Raw garlic aqueous extract (GE) has ameliorative actions on the renin-angiotensin system in type-1 diabetes mellitus (DM); however its effects on plasma and kidney angiotensin I converting enzyme type-1 (ACE-1) and angiotensin II (AngII) require further elucidation. This study investigated the effect of GE on plasma and kidney ACE-1 and AngII concentrations and in relation to systemic and renal clearance indicators significant to blood pressure (BP) homeostasis in early streptozotocin- (STZ-) induced type-1 DM. Normal rats (n=10) received 0.5 mL normal saline (NR/NS), diabetic rats (n=10) received 0.5 mL NS (DR/NS), and treated diabetic rats (n=10) received 50 mg/0.1 mL/100 g body weight GE (DR/GE) as daily intraperitoneal injections for 8 weeks. Compared to NR/NS, DR/NS showed a significant increase in plasma ACE-1 and AngII and conversely a decrease in kidney ACE-1 and AngII. These changes were associated with an increase in BP and clearance functions. Alternatively and compared to DR/NS, DR/GE showed normalization or attenuation in plasma and kidney ACE-1 and AngII. These GE induced rectifications were associated with moderation in BP elevation and renal clearance functions. Garlic attenuates modulations in plasma and kidney ACE-1 and AngII, in addition to BP and renal clearance function in type-1 DM.

scholarly journals Hypokalemia and Clinical Implications in Patients with Coronavirus Disease 2019 (COVID-19)

2020 ◽  
Author(s):  
Dong Chen ◽  
Xiaokun Li ◽  
Qifa Song ◽  
Chenchan Hu ◽  
Feifei Su ◽  
...  
Keyword(s):  
Gastrointestinal Symptoms ◽  
Renin Angiotensin System ◽  
Good Prognosis ◽  
Clinical Implications ◽  
Converting Enzyme ◽  
Angiotensin I ◽  
Angiotensin System ◽  
Angiotensin I Converting Enzyme ◽  
Underlying Causes ◽  
The Relationship

BACKGROUNDSARS-CoV-2 has caused a series of COVID-19 globally. SARS-CoV-2 binds angiotensin I converting enzyme 2 (ACE2) of renin–angiotensin system (RAS) and causes prevalent hypokalemiaMETHODSThe patients with COVID-19 were classified into severe hypokalemia, hypokalemia, and normokalemia group. The study aimed to determine the relationship between hypokalemia and clinical features, the underlying causes and clinical implications of hypokalemia.RESULTSBy Feb 15, 2020, 175 patients with COVID-19 (92 women and 83 men; median age, 46 [IQR, 34–54] years) were admitted to hospital in Wenzhou, China, consisting 39 severe hypokalemia-, 69 hypokalemia-, and 67 normokalemia patients. Gastrointestinal symptoms were not associated with hypokalemia among 108 hypokalemia patients (P > 0.05). Body temperature, CK, CK-MB, LDH, and CRP were significantly associated with the severity of hypokalemia (P<0.01). 93% of severe and critically ill patients had hypokalemia which was most common among elevated CK, CK-MB, LDH, and CRP. Urine K+ loss was the primary cause of hypokalemia. 1 severe hypokalemia patients was given 3 g/day, adding up to an average of 34 (SD=4) g potassium during hospital stay. The exciting finding was that patients responded well to K+ supplements when they were inclined to recovery.CONCLUSIONSHypokalemia is prevailing in patients with COVID-19. The correction of hypokalemia is challenging because of continuous renal K+ loss resulting from the degradation of ACE2. The end of urine K+ loss indicates a good prognosis and may be a reliable, in-time, and sensitive biomarker directly reflecting the end of adverse effect on RAS system.

Vasopressin contributes to maintenance of arterial blood pressure in dehydrated baboons

1989 ◽  
Vol 256 (2) ◽  
pp. H486-H492
Author(s):  
K. L. Ryan ◽  
R. M. Thornton ◽  
D. W. Proppe
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Enzyme Inhibitor ◽  
Renin Angiotensin System ◽  
Angiotensin I ◽  
Angiotensin System ◽  
Angiotensin I Converting Enzyme ◽  
Arterial Blood ◽  
Intact Condition

This study primarily sought to determine whether the role of vasopressin (VP) in maintenance of arterial blood pressure is enhanced in awake, chronically instrumented baboons after 68-72 h of dehydration. This question was approached by pharmacologically blocking vasopressin V1-receptors in euhydrated and dehydrated baboons with or without a normally functioning renin-angiotensin system (RAS). VP blockade during dehydration produced a rapidly occurring (within 5 min), statistically significant (P less than 0.05) decrease in mean arterial pressure (MAP) of 5 +/- 1 mmHg in the RAS-intact condition and an identical decline in MAP (5 +/- 1 mmHg) during blockade of the RAS by captopril, an angiotensin I-converting enzyme inhibitor. At 15 min after induction of VP blockade, heart rate was elevated by 9 +/- 2 beats/min in the RAS-intact condition and by 20 +/- 5 beats/min in the RAS-blocked condition. In addition, VP blockade in the dehydrated state produced small and equal increases in hindlimb vascular conductance in RAS-intact and RAS-blocked conditions. None of these cardiovascular changes were produced by VP blockade in the euhydrated state. RAS blockade produced modest declines in MAP in both hydration states, but the fall was larger by 7 +/- 4 mmHg in the dehydrated state. Thus both VP and the RAS contribute to the maintenance of arterial blood pressure during dehydration in the conscious baboon.

Effect of arginine : lysine ratio in free amino acid and protein form onl-NAME induced hypertension in hypercholesterolemic Wistar rats

RSC Advances ◽  
2016 ◽  
Vol 6 (77) ◽  
pp. 73388-73398 ◽  
Author(s):  
Vishwanath S. Vallabha ◽  
Arun Tapal ◽  
Shinde Vijay Sukhdeo ◽  
Govindaraju K ◽  
Purnima Kaul Tiku
Keyword(s):  
Free Amino ◽  
Wistar Rats ◽  
Renin Angiotensin System ◽  
Converting Enzyme ◽  
Angiotensin I ◽  
Angiotensin System ◽  
Angiotensin I Converting Enzyme ◽  
Oxide Precursor ◽  
System P ◽  
Induced Hypertension

Arginine : lysine in the ratio of 5 : 1 plays an important role in cardiovascular diseases, especially as a nitric oxide precursor leading to vasodilation and inhibiting angiotensin-I converting enzyme in renin angiotensin system.

Renin-angiotensin system inhibitors, angiotensin I-converting enzyme gene insertion/deletion polymorphism, and cancer

Cancer ◽  
2008 ◽  
Vol 112 (4) ◽  
pp. 748-757 ◽  
Author(s):  
Ronald van der Knaap ◽  
Claire Siemes ◽  
Jan-Willem W. Coebergh ◽  
Cornelia M. van Duijn ◽  
Albert Hofman ◽  
...  
Keyword(s):  
Renin Angiotensin System ◽  
Converting Enzyme ◽  
Angiotensin I ◽  
Deletion Polymorphism ◽  
Angiotensin System ◽  
Enzyme Gene ◽  
Renin Angiotensin ◽  
Gene Insertion ◽  
Angiotensin I Converting Enzyme

scholarly journals Effects of Angiotensin I-Converting Enzyme Inhibitory Substances Derived from Indonesian Dried-salted fish on Blood Pressure of Rats

1995 ◽  
Vol 59 (3) ◽  
pp. 425-429 ◽  
Author(s):  
Made Astawan ◽  
Mita Wahyuni ◽  
Tadashi Yasuhara ◽  
Kazuhiro Yamada ◽  
Tadahiro Tadokoro ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Converting Enzyme ◽  
Angiotensin I ◽  
Salted Fish ◽  
Angiotensin I Converting Enzyme

Effect of enalapril (MK-421), an orally active angiotensin I converting enzyme inhibitor, on blood pressure, active and inactive plasma renin, urinary prostaglandin E2, and kallikrein excretion in conscious rats

1984 ◽  
Vol 62 (1) ◽  
pp. 116-123 ◽  
Author(s):  
Ernesto L. Schiffrin ◽  
Jolanta Gutkowska ◽  
Gaétan Thibault ◽  
Jacques Genest
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Ace Inhibition ◽  
Renin Activity ◽  
Prostaglandin E ◽  
Converting Enzyme ◽  
Angiotensin I ◽  
Angiotensin I Converting Enzyme

The angiotensin I converting enzyme (ACE) inhibitor enalapril (MK-421), at a dose of 1 mg/kg or more by gavage twice daily, effectively inhibited the pressor response to angiotensin I for more than 12 h and less than 24 h. Plasma renin activity (PRA) did not change after 2 or 4 days of treatment at 1 mg/kg twice daily despite effective ACE inhibition, whereas it rose significantly at 10 mg/kg twice daily. Blood pressure fell significantly and heart rate increased in rats treated with 10 mg/kg of enalapril twice daily, a response which was abolished by concomitant angiotensin II infusion. However, infusion of angiotensin II did not prevent the rise in plasma renin. Enalapril treatment did not change urinary immunorcactive prostaglandin E2 (PGE2) excretion and indomethacin did not modify plasma renin activity of enalapril-treated rats. Propranolol significantly reduced the rise in plasma renin in rats receiving enalapril. None of these findings could be explained by changes in the ratio of active and inactive renin. Water diuresis, without natriuresis and with a decrease in potassium urinary excretion, occurred with the higher dose of enalapril. Enalapril did not potentiate the elevation of PRA in two-kidney one-clip Goldblatt hypertensive rats. In conclusion, enalapril produced renin secretion, which was in part β-adrenergically mediated. The negative short feedback loop of angiotensin II and prostaglandins did not appear to be involved. A vasodilator effect, apparently independent of ACE inhibition, was found in intact conscious sodium-replete rats.

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