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Related Concept Videos

Hypertension and Regulation of Blood Pressure01:18

Hypertension and Regulation of Blood Pressure

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Hypertension, the most common cardiovascular disease, is diagnosed through repeated measurements of elevated blood pressure. Its risks, including damage to the kidney, heart, and brain, are directly proportional to blood pressure levels. Starting from 115/75 mm Hg, the risk of cardiovascular disease doubles with each increment of 20/10 mm Hg. The diagnosis relies on blood pressure measurements, not on patient symptoms, as hypertension is often asymptomatic until end-organ damage is imminent or...
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Hypertension II: Pathophysiology01:29

Hypertension II: Pathophysiology

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Hypertension is a chronic condition in which the blood's force against artery walls is excessively high, posing risks such as heart disease. The condition's underlying mechanisms involve complex interactions among the cardiovascular, kidney, and autonomic nervous systems.Renin-Angiotensin-Aldosterone System (RAAS): This system significantly influences blood pressure regulation. When blood pressure decreases, the kidneys secrete renin. This enzyme transforms angiotensinogen, a plasma protein,...
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Antihypertensive Drugs: Angiotensin II Receptor Blockers01:30

Antihypertensive Drugs: Angiotensin II Receptor Blockers

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In the renin-angiotensin-aldosterone system, a hormone called angiotensin II plays a crucial role. It binds to the AT1 receptors in vascular smooth muscles coupled with Gq proteins. The activation of these receptors activates an enzyme called phospholipase C, which releases two molecules: inositol trisphosphate and diacylglycerol. These molecules cause a chain reaction that leads to the phosphorylation of myosin light chains and promotes interaction between actin and myosin, leading to smooth...
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Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors01:30

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors

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Angiotensin-converting enzyme (ACE), a vital component of the renin-angiotensin-aldosterone system, is abundant in lung endothelial cells. ACE converts the inactive decapeptide, angiotensin I, into the active octapeptide, angiotensin II. This potent vasoconstrictor narrows blood vessels, increasing resistance to blood flow and elevating blood pressure. Angiotensin II also stimulates aldosterone production, encouraging kidney cells to reabsorb more sodium and water from urine, thereby increasing...
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Hypertension I: Introduction01:28

Hypertension I: Introduction

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Hypertension is a widespread, long-term medical condition where blood pressure in the arteries remains elevated. It is characterized by systolic blood pressure readings of 130 mm Hg or above or diastolic blood pressure (DBP) readings of 80 mm Hg or higher. Unmanaged hypertension poses significant health risks, making the distinction between primary (or essential) hypertension and secondary hypertension crucial, as their management and implications vary.Primary HypertensionPrimary hypertension,...
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Antihypertensive Drugs: Direct Renin Inhibitors01:25

Antihypertensive Drugs: Direct Renin Inhibitors

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The renin-angiotensin-aldosterone system (RAAS) is an intricate physiological pathway involving numerous enzymes and hormones, including renin, angiotensin-converting enzyme (ACE), angiotensin I and II, and aldosterone. Imbalances within this system increase the production of angiotensin II and aldosterone. Increased angiotensin II levels promote vasoconstriction and blood pressure elevation. Concurrently, higher aldosterone levels stimulate sodium and water reabsorption in the kidneys,...
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Simultaneous Electrocardiography Recording and Invasive Blood Pressure Measurement in Rats
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Resistant hypertension and central aortic pressure

Michael F O'Rourke1, Michel E Safar, Audrey Adji

  • 1aSt Vincent's Clinic bUniversity of New South Wales, Victor Chang Cardiac Research Institute, Sydney, New South Wales, Australia cParis Descartes University, AP-HP, Diagnosis and Therapeutic Center, Hôtel-Dieu, Paris, France dAustralian School of Advanced Medicine, Macquarie University, Sydney, New South Wales, Australia.

Journal of Hypertension
|January 31, 2014
PubMed
Summary

No abstract available in PubMed .

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