Exercise training ameliorates adrenergic control in spontaneously hypertensive rats
Munique Tostes Ferreira Miranda1,2, Marina Paiva Lemos1, Jeffer Eidi Sasaki1
1Exercise Science, Health and Human Performance Research Group, Department of Sport Sciences, Federal University of Triângulo Mineiro , Uberaba, Brazil.
Clinical and Experimental Hypertension (New York, N.Y. : 1993)
|September 14, 2020
Summary
Swimming training in hypertensive rats reduced blood pressure responses to tyramine infusion, indicating improved cardiovascular autonomic function. This suggests exercise training may attenuate hypertension-related injury through sympathetic nervous system adjustments.
Area of Science:
- Cardiovascular Physiology
- Exercise Physiology
- Autonomic Nervous System Function
Background:
- Hypertension is associated with autonomic dysfunction and increased cardiovascular risk.
- Exercise training is known to improve cardiovascular health, but its effects on sympathetic vascular control in hypertension require further investigation.
Purpose of the Study:
- To investigate the impact of swimming training on vascular control following sympathetic stimulation in hypertensive rats.
- To assess changes in arterial pressure, heart rate, and their variability after tyramine infusion in trained versus sedentary hypertensive and normotensive rats.
Main Methods:
- Male rats were divided into sedentary/trained normotensive and sedentary/trained hypertensive groups.
- Measurements included arterial pressure (AP), heart rate (HR), HR variability (HRV), and AP variability (APV).
- Tyramine infusion was administered to assess sympathetic responses, followed by analysis of autonomic modulation.
Main Results:
- Trained hypertensive rats exhibited lower resting HR, reduced AP, higher HRV, and lower APV compared to sedentary hypertensive rats.
- Both trained groups showed increased parasympathetic modulation of HRV and vagal effects.
- Tyramine-induced pressor and HR responses were significantly attenuated in trained hypertensive rats.
Conclusions:
- Exercise training in hypertensive rats leads to adjustments in sympathetic nerve endings, reducing the pressor response to tyramine.
- This attenuation of vasoconstrictor effects may mitigate hypertension-induced cardiovascular injury.
- Swimming training improves cardiovascular autonomic dysfunction in hypertensive states, potentially via sympathetic attenuation.
Related Concept Videos
01:26Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
732
The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
732
01:30Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors
2.1K
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...
2.1K
01:17Antihypertensive Drugs: Action of β1 Blockers
1.8K
β1-receptors are primarily located in the heart and kidneys. In cardiac myocytes, these receptors interact with neurotransmitters released by the sympathetic nervous system during heightened activity or danger. As a result, β1-receptors get activated, initiating a series of biochemical processes. Excessive activation of beta receptors due to chronic stress can abnormally increase heart rate and contractility, resulting in high blood pressure or hypertension. To counteract this,...
1.8K
01:29Hypertension II: Pathophysiology
538
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,...
538
01:18Hypertension and Regulation of Blood Pressure
3.5K
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...
3.5K
01:30Antihypertensive Drugs: Angiotensin II Receptor Blockers
2.2K
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...
2.2K