13.6 Lecture Pressure Diuresis and Natriuresis

When arterial pressure increases, the kidneys increase water output which is known as pressure diuresis.

There is an approximate, equal increase in sodium output, called pressure natriuresis.

At 50 arterial pressure, urinary output is essentially zero.

At 100 arterial pressure, urinary output is normal.

At 200 arterial pressure, urinary output is four to six times normal demonstrating that as arterial pressure rises, urinary output also rises.

In the long term, output must equal intake, in order for long term change to occur, equilibrium point has to change.

Chronic changes in arterial pressure have a much greater effect on renal output of salt and water than acute changes.

This means that the chronic renal output curve is much steeper than the acute curve.

The indirect effect of hypertension is increased renal blood flow, which causes increased urinary output indirectly.

There is a decrease sympathetic stimulation causing decreased norepinephrine release.

If the kidneys and the nervous system are functioning normally, chronic increases in salt and water intake have very a little effect on blood pressure.

People with kidney injury or excessive secretion of antidiuretic hormone are more salt sensitive.

As long as hormonal and renal function are normal, urinary output changes greatly with salt intake.

Blood pressure equals cardiac output times peripheral vascular resistance.

If the kidneys are functioning normally, pressure decreases naturally occurs within a few hours of blood pressure increases without a subsequent rise in resistance.

Increases in total peripheral resistance, typically increase intra renal vascular pressure at the same time, which then alters kidney function.

Diuresis and natriuresis are intimately tied with blood pressure.

Increased blood pressure is caused through increased preload, creating increased cardiac output, which causes increased peripheral vascular resistance.

If blood pressure and therefore blood flow increase, auto regulation will cause constriction to regulate flow and therefore an increase in peripheral vascular resistance.

If blood pressure increases, flow increases and there is an immediate response from the local tissue level that will decrease or increase constriction, which decreases flow.

Hypertension causes shortened life expectancy caused by excessive workload of the heart, high pressure that damages blood vessels in the brain causing a CVA and hypertension, causing injury to the kidneys and ultimately, kidney failure.

Volume loading with decreased kidney function, initially causes increased cardiac output, but within a few weeks, there's an increase in peripheral vascular resistance and cardiac output is returned to normal.

The pair of centers have been reset and hypertension ensues as peripheral vascular resistance increases and cardiac output as well as extracellular fluid volume decreases, yet blood pressure remains elevated.

Volume lowering hypertension can be caused by excessive aldosterone or excesses of other steroids.

Peripheral vascular resistance and hypertension are the endpoint.

Justo glomerular cells are located mainly in the walls of arterials, and they release renin in response to decreased pressure, decreased osmolality at the macula, denser, and increased sympathetic nervous system activity.

Renin acts in semantically on angiotensin two release angiotensin one from which two amino acids are split to form angiotensin two.

Angiotensin converting enzyme, or ACE, is present in editing of tissue of the lungs.

Angiotensin two has a very short lifespan, because it is rapidly inactivated, but is extremely powerful vasoconstrictor that acts by directly causing vasoconstriction, and secondarily causing stimulation of aldosterone secretion, which causes renal tubule salt and water reabsorption.

Whenever angiotensin two circulates, it causes a resetting of the arteries pressure and renal output curve.

Angiotensin two decreases renal flow by acting directly on the renal arterials, especially the arterial, to cause constriction.

This decreases pressure, which causes increased sodium and water reabsorption.

Indirectly, angiotensin two causes aldosterone secretion, causing sodium and water reabsorption.

Higher angiotensin levels result in higher blood pressure effects.

Primary hypertension means hypertension of unknown origin, not secondarily to known causes such as renal artery analysis.

Excessive weight gain, and sedentary lifestyle are major determining factors.

Excessive weight gain causes increased cardiac output, partially caused by increased blood flow demands.

Increased blood flow caused by increased cardiac output is eventually normalized by increased peripheral vascular resistance.

Increased sympathetic activity has multiple theories, but it does cause the elevation of angiotensin two levels.

There's a resetting of the normal renal pressure natriuresis mechanism to a higher set point, causing increased sodium and water retention.

Treatment of a central hypertension is typically through vasodilator drugs because increase renal blood flow, uh, and natural excess or diuretic drugs, which decrease tubular reabsorption of salt and water.

Arterial pressure is regulated by several interrelated systems that differ in their acute and chronic utilizations.

Acute dynamic control typically uses the barrier receptor feedback mechanism, the CNS mechanism, and the chemo receptor mechanism which act to cause final venous constriction, increase heart rate and contractility, and peripheral arterial constriction.

Chronic systems include the renin angiotensin vasoconstrictor, mechanism of stress, relaxation of the vasculature, and intravascular and intracellular fluid shifts, causing readjustment of blood volume.

Decreasing blood pressure or a capillary hydrostatic pressure caused reabsorption of fluid from the interstitium.