Effects of ANG II and III and angiotensin receptor blockers on nasal salt gland secretion and arterial blood pressure in conscious Pekin ducks ( Anas platyrhynchos )

1998 ◽  
Vol 168 (3) ◽  
pp. 213-224 ◽  
Author(s):  
D. G. Butler ◽  
R. Zandevakili ◽  
G. Y. Oudit
2005 ◽  
Vol 6 (1_suppl) ◽  
pp. S8-S11
Author(s):  
Hans-Christoph Diener

Hypertension is the most important modifiable risk factor for primary and secondary stroke prevention. All antihypertensive drugs are effective in primary prevention: the risk reduction for stroke is 30—42%. However, not all classes of drugs have the same effects: there is some indication that angiotensin receptor blockers may be superior to other classes of antihypertensive drugs in stroke prevention. Seventy-five percent of patients who present to hospital with acute stroke have elevated blood pressure within the first 24—48 hours. Extremes of systolic blood pressure (SBP) increase the risk of death or dependency. The aim of treatment should be to achieve and maintain the SBP in the range 140—160 mmHg. However, fast and drastic blood pressure lowering can have adverse consequences. The PROGRESS trial of secondary prevention with perindopril + indapamide versus placebo + placebo showed a decrease in numbers of stroke recurrences in patients given both active antihypertensive agents, more impressive for cerebral haemorrhage.There were also indications that active treatment might decrease the development of post-stroke dementia.


2021 ◽  
Vol 54 (3) ◽  
pp. 275-276
Author(s):  
Kanwal Ashiq ◽  
Sana Ashiq

Dear Editor, In December 2019, a new virus which is known as SARS-COV-2 (COVID-19) was identified. In a short period, this virus spread rapidly and caused significant morbidities and mortalities across the earth. On March 11, 2020, the World Health Organization (WHO) declared a pandemic due to the logarithmic expansion of COVID-19 cases globally.1 Various guidelines were issued, and a complete lockdown has been observed on a large scale to stop the spread of the virus. Currently, there is no specific treatment for COVID-19 is available. Throughout the year 2020, scientists struggled a lot to find the COVID-19 cure, and many vaccines are successfully developed which would be helpful in the prevention of disease. Nevertheless, the emergence of virus variants remains an issue. The epidemiological trends and clinical features of this disease have been reported in several publications.2 Due to comorbidities, COVID-19 disease can exacerbate and may result in increased severity and deadly consequences. In a study, the most common comorbidities in COVID-19 patients were reported as following; diabetes (19%), hypertension (30%), and coronary heart disease (8%). In hypertension, blood pressure elevates from the threshold level. The occurrence of hypertension is not necessarily to be associated with COVID-19 as hypertension is quite frequent in geriatric patients, and these patients are at higher risk of being infected with COVID-19.3,4 Angiotensin receptor blockers (ARBs) and angiotensin-converting enzyme (ACE) inhibitors are widely prescribed for the cure of hypertension and other cardiovascular-related diseases. On the other hand, the COVID-19 virus binds with ACE2 to gain entry into the lung cells. ACE inhibitors and ARBs escalate ACE2 that could hypothetically increase the chance of COVID-19 binding to lung cells and could headway to more damage. Conversely, in experimental studies, ACE2 showed a protective effect against lung injury. Due to the anti-inflammatory potential of ACE inhibitors and ARBs, these agents can reduce the incidence of developing myocarditis and acute respiratory distress syndrome in COVID-19 patients. There is no evidence that hypertension is linked with the COVID-19 and anti-hypertensive medicines (ACE inhibitors and ARBs) are either harmful or beneficial during the COVID-19 pandemic.5 During this unprecedented situation, the Council on Hypertension of the European Society of Cardiology released a statement that “The Council on Hypertension strongly recommends that physicians and patients should continue treatment with their usual anti-hypertensive therapy because there is no clinical or scientific evidence to suggest that treatment with ACEIs or ARBs should be discontinued because of the COVID-19 infection.” After this announcement, many other societies also recommend that patients should continue using their current hypertensive therapy and if necessary, after careful assessment, changes can be made in the hypertensive regimen.6 According to estimation, globally, 1.5 billion people can suffer from hypertension by 2025 which may contribute approximately 75% of stroke risk and 50% of heart disease risk. CVDs accounts almost 38% of deaths related to the non-communicated disease (NCDs). In Pakistan, hypertension is a chief health concern that leads to significant morbidity and mortality. Blood pressure can be control with medications and lifestyle modifications. One of the best approaches to control and improve blood pressure is team-based care consisting of doctors, pharmacists, and nurses. During COVID-19, collaborative efforts are required to improve patient’s quality of life and to reduce the healthcare burden.7,8 Keywords: COVID-19, Hypertension, Pandemic, ACE inhibitors References Ashiq K, Bajwa MA, Ashiq S. COVID-19 Pandemic and its Impact on Pharmacy Education. Turkish J Pharma Sci. 2021;18(2):122. Ashiq K, Ashiq S, Bajwa MA, Tanveer S, Qayyum M. Knowledge, attitude and practices among the inhabitants of Lahore, Pakistan towards the COVID-19 pandemic: an immediate online based cross-sectional survey while people are under the lockdown. Bangladesh J Med Sci. 2020:69-S 76. Zhou F, Yu T, Du R, Fan G, Liu Y, Liu Z, et al. Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study. Lancet. 2020;395(10229):1054-62. Ashiq S, Ashiq K. The Role of Paraoxonase 1 (PON1) Gene Polymorphisms in Coronary Artery Disease: A Systematic Review and Meta-Analysis. Biochem Genet. 2021:1-21. Schiffrin EL, Flack JM, Ito S, Muntner P, Webb RC. Hypertension and COVID-19. Am J Hypertens. 2020;33(5):373–374. Patel AB, Verma A. COVID-19 and angiotensin-converting enzyme inhibitors and angiotensin receptor blockers: what is the evidence? JAMA. 2020;323(18):1769-70. Riaz M, Shah G, Asif M, Shah A, Adhikari K, Abu-Shaheen A. Factors associated with hypertension in Pakistan: A systematic review and meta-analysis. PLoS One. 2021;16(1):e0246085. Zarei L, Karimzadeh I, Moradi N, Peymani P, Asadi S, Babar Z-U-D. Affordability assessment from a static to dynamic concept: a scenario-based assessment of cardiovascular medicines. Int J Environ Res Public Health. 2020;17(5):1710.


1993 ◽  
Vol 265 (3) ◽  
pp. R591-R595 ◽  
Author(s):  
R. L. Thunhorst ◽  
S. J. Lewis ◽  
A. K. Johnson

Intracerebroventricular (icv) infusion of angiotensin II (ANG II) in rats elicits greater water intake under hypotensive, compared with normotensive, conditions. The present experiments used sinoaortic baroreceptor-denervated (SAD) rats and sham-operated rats to examine if the modulatory effects of arterial blood pressure on water intake in response to icv ANG II are mediated by arterial baroreceptors. Mean arterial blood pressure (MAP) was raised or lowered by intravenous (i.v.) infusions of phenylephrine (1 or 10 micrograms.kg-1 x min-1) or minoxidil (25 micrograms.kg-1 x min-1), respectively. The angiotensin-converting enzyme inhibitor captopril (0.33 mg/min) was infused i.v. to prevent the endogenous formation of ANG II during testing. Urinary excretion of water and solutes was measured throughout. Water intake elicited by icv ANG II was inversely related to changes in MAP. Specifically, rats drank more water in response to icv ANG II when MAP was reduced by minoxidil but drank less water when MAP was elevated by phenylephrine. The influence of changing MAP on the icv ANG II-induced drinking responses was not affected by SAD. These results suggest that the modulatory effects of arterial blood pressure on icv ANG II-induced drinking can occur in the absence of sinoaortic baroreceptor input.


2019 ◽  
Vol 40 (12) ◽  
pp. 756-761
Author(s):  
Miguel Ramirez-Jimenez ◽  
Felix Morales-Palomo ◽  
Juan Fernando Ortega ◽  
Ricardo Mora-Rodriguez

AbstractWe studied the effects of supramaximal interval exercise (SIE) with or without antihypertensive medication (AHM) on 21-hr blood pressure (BP) response. Twelve hypertensive patients chronically medicated with AHM, underwent three trials in a randomized order: a) control trial without exercise and substituting their AHM with a placebo (PLAC); b) placebo medicine and a morning bout of SIE (PLAC+SIE), and c) combining AHM and exercise (AHM+SIE). Acute and ambulatory blood pressure responses were measured for 21-hr after treatment. 20  min after treatment, systolic blood pressure (SBP) readings were reduced, similar to readings after PLAC+SIE (−9.7±6.0 mmHg, P<0.001) and AHM+SIE (−10.4±7.9 mmHg, P=0.001). 21 h after treatment, SBP remained reduced after PLAC+SIE (125±12 mmHg, P=0.022) and AHM+SIE (122±12 mmHg, P=0.013) compared to PLAC (132±16 mmHg). The BP reduction in PLAC+SIE faded out at 4 a.m., while in AHM+SIE it continued overnight. At night, BP reduction was larger in AHM+SIE than PLAC+SIE (–5.6±4.0 mmHg, P=0.006). Our data shows that a bout of supramaximal aerobic interval exercise in combination with ARB medication in the morning elicits a sustained blood pressure reduction lasting at least 21-h. Thus, the combination of exercise and angiotensin receptor blocker medication seems superior to exercise alone for acutely decreasing blood pressure.


1982 ◽  
Vol 62 (1) ◽  
pp. 51-56 ◽  
Author(s):  
R. Hatton ◽  
D. P. Clough ◽  
S. A. Adigun ◽  
J. Conway

1. Lower-body negative pressure (LBNP) was used to stimulate sympathetic reflexes in anaesthetized cats. At −50 mmHg for 10 min it caused transient reduction in central venous pressure and systemic arterial blood pressure. Arterial blood pressure was then restored within 30 s and there was a tachycardia. Central venous pressure showed only partial recovery. The resting level of plasma renin activity (PRA; 2.9–3.2 ng h−1 ml−1) did not change until approximately 5 min into the manoeuvre. 2. When converting-enzyme inhibitor (CEI) was given 75 s after the onset of suction it caused a greater and more sustained fall in arterial blood pressure than when administered alone. The angiotensin II (ANG II) antagonist [Sar1,Ala8]ANG II produced similar effects after a short-lived pressor response. 3. This prolonged fall in arterial blood pressure produced by CEI was not associated with reduced sympathetic efferent nerve activity. This indicates that the inhibitor affects one of the peripheral actions of angiotensin and in so doing produces vasodilatation of neurogenic origin. 4. These findings suggest that angiotensin, at a level which does not exert a direct vasoconstrictor action, interacts with the sympathetic nervous system to maintain arterial blood pressure when homeostatic reflexes are activated. A reduction in the efficiency of these reflexes by CEI may contribute to its hypotensive effect.


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