Dietary nitrate does not alter cardiac function, calcium handling proteins, or SERCA activity in the left ventricle

Aleah J Kirsh1, Emma S Juracic2, Heather L Petrick1

  • 1Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, ON, Canada.

Insights

Dietary nitrate supplementation reduced blood pressure in rats but did not affect heart calcium handling or SERCA activity. This suggests nitrate does not impact cardiac relaxation mechanisms in healthy hearts.

Area of Science:

  • Cardiovascular Physiology
  • Nutritional Biochemistry

Background:

  • Dietary nitrate intake is linked to potential cardiovascular benefits.
  • Increased cytosolic calcium in the heart necessitates enhanced calcium sequestration for proper relaxation.

Purpose of the Study:

  • To investigate the effects of dietary nitrate on cardiac calcium handling and SERCA activity in healthy rats.
  • To determine if nitrate supplementation impacts left ventricular function and blood pressure.

Main Methods:

  • Rats were supplemented with dietary nitrate.
  • Measurements included blood pressure, left ventricular function, calcium-handling protein content, and SERCA enzymatic activity.
  • In vitro assays assessed SERCA activity directly.

Main Results:

  • Nitrate supplementation significantly reduced blood pressure.
  • No significant alterations were observed in calcium-handling protein content, SERCA enzymatic properties, or left ventricular function.
  • In vitro SERCA activity remained unchanged by nitrite exposure.

Conclusions:

  • Dietary nitrate effectively lowers blood pressure in healthy rats.
  • Nitrate supplementation does not enhance or impair left ventricular SERCA-related calcium-handling properties in this model.
  • These findings indicate that nitrate's cardiovascular benefits may not involve direct modulation of cardiac SERCA function.

Related Concept Videos

Antianginal Drugs: Nitrates and β-Blockers01:16

Antianginal Drugs: Nitrates and β-Blockers

In cardiovascular health, antianginal drugs combat angina pectoris — a condition marked by chest pain owing to diminished blood flow to the heart.
Organic nitrates,  such as nitroglycerin, play a pivotal role. Once metabolized, they liberate nitric oxide, a molecular marvel. Nitric oxide triggers guanylyl cyclase and augments cGMP production. This biochemical cascade orchestrates the relaxation of vascular smooth muscles, ushering in vasodilation and enhancing coronary blood flow....
1.2K
Nitric Oxide Signaling Pathway01:28

Nitric Oxide Signaling Pathway

Nitric oxide (NO), an inorganic gas, acts as a potent second messenger in most animal and plant tissues. NO diffuses out of the cells that produce it and enters the neighboring cells to generate a downstream response. NO synthase (NOS) catalyzes NO production by the deamination of the amino acid arginine. There are three isoforms of NOS. Endothelial cells have endothelial NOS (eNOS), nerve and muscle cells have neuronal NOS (nNOS), and macrophages produce inducible NOS (iNOS) upon exposure...
6.0K
Antianginal Drugs: Calcium Channel Blockers and Ranolazine01:25

Antianginal Drugs: Calcium Channel Blockers and Ranolazine

Angina pectoris, a primary symptom of ischemic heart disease, requires careful pharmacological interventions. In this context, calcium channel blockers (CCBs) and ranolazine have emerged as crucial pharmacotherapeutic agents, providing deep insights into the complexities of angina management.
CCBs, a diverse class that includes dihydropyridines (nifedipine) and diphenylalkylamines (verapamil and diltiazem), exert their effect by blocking calcium channels in cardiac and smooth muscle cells. This...
1.1K
Antihypertensive Drugs: Action of Calcium Channel Blockers01:18

Antihypertensive Drugs: Action of Calcium Channel Blockers

Calcium ions are essential to contract smooth muscle cells in blood vessels. They enter these cells through voltage-dependent calcium channels, specifically L-type calcium channels in the cell membrane. These L-type calcium channels are integral to the excitation-contraction coupling process in smooth muscle. When a stimulus is received by smooth muscle cells, their membrane depolarizes. This alteration in membrane potential instigates the opening of L-type calcium channels. As a result,...
1.4K
2° Amines to N-Nitrosamines: Reaction with NaNO201:20

2° Amines to N-Nitrosamines: Reaction with NaNO2

Secondary amines react with nitrous acid to form N-nitrosamines, as depicted in Figure 1. Nitrous acid, a weak and unstable acid, is formed in situ from an aqueous solution of sodium nitrite and strong acids, such as hydrochloric acid or sulfuric acid, in cold conditions. In the presence of an acid, the nitrous acid gets protonated. The subsequent loss of water results in the formation of the electrophile known as nitrosonium ion.
5.2K
Antihypertensive Drugs: Vasodilators01:23

Antihypertensive Drugs: Vasodilators

Vasodilators, primarily affecting the smooth muscles within arterial and venous walls, are commonly used for hypertension treatment. Medications such as minoxidil and hydralazine primarily target arteries and arterioles, while sodium nitroprusside acts on arterioles and venules. Minoxidil, functioning as a prodrug, is metabolized by hepatic sulfotransferase into its active form, minoxidil sulfate, after oral administration. This metabolite binds to the sulfonylurea receptor (SUR) component of...
1.9K