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Related Concept Videos

Hormonal Regulation01:33

Hormonal Regulation

The renin-aldosterone system is an endocrine system which guides the renal absorption of water and electrolytes, thus managing blood pressure and osmoregulation. Activation of the system begins in the kidneys with a small cluster of cells adjacent to the afferent and efferent blood vessels of the renal corpuscle. As the nephrons are filtering blood, juxtaglomerular cells monitor blood pressure. If they detect a decrease in pressure, they release the hormone renin into the bloodstream.
Hypertension and Regulation of Blood Pressure01:18

Hypertension and Regulation of Blood Pressure

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...
Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors01:30

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors

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...
Pharmacogenetics of Drug Transporters: P-Glycoprotein and Solute Carrier Transporters01:16

Pharmacogenetics of Drug Transporters: P-Glycoprotein and Solute Carrier Transporters

The pharmacogenetics of drug transporters is increasingly recognized as a critical factor influencing interindividual variability in drug absorption, distribution, and elimination. These membrane-bound proteins regulate drugs' movement across cellular barriers by actively pumping them out (efflux) or facilitating their uptake (influx). Among the major transporter families, ATP-binding cassette (ABC) and solute carrier (SLC) transporters play particularly prominent roles. Genetic polymorphisms...
Hypertension II: Pathophysiology01:29

Hypertension II: Pathophysiology

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,...
Diabetic Nephropathy01:28

Diabetic Nephropathy

Definition Diabetic nephropathy is a chronic kidney complication that results from prolonged hyperglycemia.Prevalence It is the most common cause of chronic kidney disease (CKD) and end-stage renal disease (ESRD) worldwide, affecting up to half of individuals with diabetes.Pathophysiology • Sustained hyperglycemia triggers multiple hemodynamic and metabolic changes in the kidney. • Early in the disease, increased renal blood flow and glomerular hyperfiltration occur due to afferent arteriolar...

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Related Experiment Video

Updated: Jul 13, 2026

Microperfusion Technique to Investigate Regulation of Microvessel Permeability in Rat Mesentery
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Published on: September 12, 2015

ACE gene insertion/deletion polymorphism modulates capillary permeability in hypertension.

Giulia Dell'omo1, Giuseppe Penno, Laura Pucci

  • 1Dipartimento Cardio Toracico, Università di Pisa, Pisa, Italy.

Clinical Science (London, England : 1979)
|August 8, 2006
PubMed
Summary

The ACE D/D gene variant is linked to increased systemic capillary permeability in hypertensive men, suggesting a genetic factor in atherosclerosis risk. This finding highlights potential genetic influences on microvascular abnormalities in hypertension.

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Area of Science:

  • Cardiovascular Genetics
  • Vascular Biology
  • Hypertension Research

Background:

  • The angiotensin 1-converting enzyme (ACE) D/D genotype is associated with increased microalbuminuria and atherosclerotic vascular disease risk in essential hypertension.
  • It remains unclear if this genetic profile correlates with altered systemic capillary endothelial permeability or generalized endothelial dysfunction.

Purpose of the Study:

  • To investigate the association between ACE gene polymorphism (D/D vs. I/I or I/D) and systemic capillary permeability in never-treated essential hypertensive men.
  • To evaluate if the ACE D/D genotype influences transcapillary escape rate of albumin (TERalb) and albuminuria.

Main Methods:

  • ACE gene polymorphism determined by PCR in 79 hypertensive men and 16 normotensive controls.
  • Systemic capillary permeability assessed by TERalb (1-h decline rate of intravenous (125)I-albumin).
  • Evaluated albuminuria, forearm vasodilation to acetylcholine, blood pressure, metabolic status, and smoking habits.

Main Results:

  • TERalb was significantly higher in hypertensive men with the ACE D/D genotype compared to I/D and I/I genotypes.
  • D/D homozygotes exhibited higher albuminuria and more frequent microalbuminuria.
  • Forearm vasodilation, fasting glucose, insulin sensitivity, and metabolic parameters did not differ between genotype groups.

Conclusions:

  • ACE D/D homozygosis is independently associated with increased TERalb in essential hypertensive men, indicating heightened systemic vascular permeability.
  • This suggests a potential genetic contribution to atherogenesis via microvascular abnormalities, independent of impaired nitric oxide-mediated vasodilation.
  • The parallel increase in TERalb and albuminuria suggests shared genetic determinants for renal and systemic microvascular dysfunction in hypertension.