what enzyme produced by the kidneys helps to regulate blood pressure?

Regulation of Blood Volume by the Kidneys

The formation of urine begins in the same manner as the formation of tissue fluid—by filtration of plasma through capillary pores. These capillaries are known as glomeruli, and the filtrate they produce enters a arrangement of tubules that transports and modifies the filtrate (by mechanisms discussed in chapter 17). The kidneys produce well-nigh 180 L per day of blood filtrate, only since at that place is merely v.five 50 of blood in the body, it is clear that most of this filtrate must be returned to the vascular system and recycled. Only about 1.5 L of urine is excreted daily; 98% to 99% of the corporeality filtered is reabsorbed back into the vascular system.

The book of urine excreted can exist varied by changes in the reabsorption of filtrate. If 99% of the filtrate is reabsorbed, for case, 1% must be excreted. Decreasing the reabsorption by just 1%—from 99% to 98%—would double the volume of urine excreted (an increment to 2% of the amount filtered). Conveying the logic farther, a doubling of urine book from, for example, 1 to 2 liters, would event in the loss of an additional liter of blood book. The percentage of the glomerular filtrate reabsorbed—and thus the urine volume and claret volume—is adjusted according to the needs of the body by the activeness of specific hormones on the kidneys. Through their effects on the kidneys, and the resulting changes in blood volume, these hormones serve important functions in the regulation of the cardiovascular system.

Regulation by Antidiuretic Hormone (ADH)

One of the major hormones involved in the regulation of blood book is antidiuretic hormone (ADH), also known as vaso-pressin. Equally described in affiliate xi, this hormone is produced by neurons in the hypothalamus, transported past axons into the posterior pituitary, and released from this storage gland in response to hypothalamic stimulation. The release of ADH from the posterior pituitary occurs when neurons in the hypothalamus called osmoreceptors notice an increase in plasma osmolality (osmotic pressure).

An increment in plasma osmolality occurs when the plasma becomes more concentrated (chapter vi). This can be produced either by aridity or by excessive salt intake. Stimulation of osmoreceptors produces sensations of thirst, leading to increased water intake and an increase in the amount of ADH released from the posterior pituitary. Through mechanisms that will exist discussed in conjunction with kidney physiology in chapter 17, ADH stimulates water reabsorption from the filtrate. A smaller book of urine is thus excreted equally a result of the activity of ADH (fig. 14.11).

A person who is dehydrated or who consumes excessive amounts of table salt thus drinks more than and urinates less. This raises the claret volume and, in the process, dilutes the plasma to lower its previously elevated osmolality. The rising in claret volume that results from these mechanisms is extremely important in stabilizing the status of a dehydrated person with low blood volume and pressure.

Osmoreceptors in hypothalamus

Posterior Thirst pituitary

Posterior Thirst pituitary t ADH

Water memory '

Water memory '

responses J Blood osmolality

■ Figure 14.11 The negative feedback control of blood volume and blood osmolality. Thirst and ADH secretion are triggered by a ascent in plasma osmolality. Homeostasis is maintained past countermeasures, including drinking and conservation of water by the kidneys.

Clinical Investigation Clues

Remember that Charlie had a depression urine output and that his urine had a loftier osmolality (concentration). What physiological mechanism could be responsible for this? What benefit does Charlie derive from this mechanism?

Drinking excessive amounts of water without excessive amounts of salt does not result in a prolonged increase in blood volume and pressure level. The water does enter the blood from the intestine and momentarily raises the claret volume; at the aforementioned time, however, it dilutes the blood. Dilution of the blood decreases the plasma osmolality and thus inhibits the release of ADH. With less ADH there is less reabsorption of filtrate in the kidneys—a larger volume of urine is excreted. H2o is therefore a diuretic—a substance that promotes urine formation—considering it inhibits the release of antidiuretic hormone.

An increase in claret volume can thus be compensated by a fall in ADH secretion. Nonetheless, expanded blood book besides

Cardiac Output, Blood Flow, and Blood Force per unit area stimulates stretch receptors in the left atrium of the eye, causing the increased secretion of a different hormone. This is a polypeptide known as atrial natriuretic peptide (discussed in a separate section shortly). This hormone promotes the increased excretion of salt and water in the urine, thereby helping to lower the blood book.

During prolonged exercise, particularly on a warm day, a substantial amount of water (up to 900 ml per hr) may be lost from the body through sweating. The lowering of claret volume that results decreases the ability of the body to dissipate heat, and the consequent overheating of the body can cause ill effects and put an end to the exercise. The need for athletes to remain well hydrated is unremarkably recognized, only drinking pure water may not be the respond. This is considering blood sodium is lost in sweat, so that a lesser corporeality of water is required to dilute the blood osmolality dorsum to normal. When the blood osmolality is normal, the urge to drinkable is extinguished. For these reasons, athletes performing prolonged endurance exercise should drink solutions containing sodium (also as carbohydrates for energy), and they should drink at a predetermined rate rather than at a charge per unit determined only by thirst.

Regulation past Aldosterone

From the preceding discussion, it is clear that a certain corporeality of dietary common salt is required to maintain blood book and pressure. Since Na+ and Cl- are easily filtered in the kidneys, a mechanism must be to promote the reabsorption and retention of common salt when the dietary salt intake is besides low. Aldosterone, a steroid hormone secreted by the adrenal cortex, stimulates the reabsorption of salt by the kidneys. Aldosterone is thus a "salt-retaining hormone." Retention of common salt indirectly promotes retention of water (in office, by the action of ADH, as previously discussed). The activity of aldosterone produces an increment in claret volume, simply, unlike ADH, it does non produce a alter in plasma osmolality. This is because aldosterone promotes the reabsorption of table salt and water in proportionate amounts, whereas ADH promotes just the reabsorption of water. Thus, different ADH, aldosterone does not human activity to dilute the claret.

The secretion of aldosterone is stimulated during salt impecuniousness, when the blood volume and pressure are reduced. The adrenal cortex, still, is not directly stimulated to secrete al-dosterone by these conditions. Instead, a decrease in claret volume and pressure level activates an intermediate mechanism, described in the next section.

Throughout most of human history, common salt was in short supply and was therefore highly valued. Moorish merchants in the sixth century traded an ounce of salt for an ounce of gold, and common salt cakes were used as money in Abyssinia. Part of a Roman soldier'due south pay was given in salt—a practice from which the give-and-take bacon (sal = table salt) derives. Salt was as well used to buy slaves—hence the phrase "worth his table salt."

Stimuli

I Blood pressure I Blood flow to kidneys

Juxtaglomerular apparatus in kidneys

Renin

Angiotensinogen

Angiotensin I ACE

Angiotensin II

Adrenal cortex

Aldosterone

Vasoconstriction of arterioles

Salt and water retention by kidneys

Salt and water memory by kidneys

■ Figure fourteen.12 The renin-angiotensin-aldosterone system. This organisation helps to maintain homeostasis through the negative feedback control of claret book and pressure. (ACE = angiotensin-converting enzyme.)

Renin-Angiotensin-Aldosterone System

When the claret flow and pressure are reduced in the renal artery (equally they would exist in the low-blood-volume country of salt deprivation), a group of cells in the kidneys called the juxtaglomerular apparatus secretes the enzyme renin into the blood. This enzyme cleaves a 10-amino-acrid polypeptide called angiotensin I from a plasma protein chosen angiotensinogen. Every bit angiotensin I passes through the capillaries of the lungs, an angiotensin-converting enzyme (ACE) removes two amino acids. This leaves an eight-amino-acrid polypeptide chosen angiotensin 2 (fig. 14.12). Conditions of common salt deprivation, low claret volume, and low blood pressure, in summary, crusade increased product of angiotensin Ii in the blood.

Angiotensin II exerts numerous furnishings that produce a rise in blood pressure. This rise in pressure is partly due to vasoconstriction and partly to increases in claret book. Vasoconstriction of arterioles and small muscular arteries is produced straight by the furnishings of angiotensin II on the smooth musculus layers of these vessels. The increased claret volume is an indirect upshot of angiotensin II.

Angiotensin II promotes a rise in blood volume by means of two mechanisms: (1) thirst centers in the hypothalamus are stimulated by angiotensin II, and thus more water is ingested, and (2) secretion of aldosterone from the adrenal cortex is stimulated by angiotensin II, and higher aldosterone secretion causes more salt and h2o to exist retained by the kidneys. The human relationship between angiotensin II and aldosterone is sometimes described as the renin-angiotensin-aldosterone system.

Clinical Investigation Clues

Remember that Charlie'southward urine had about no Na+ in it.

■ What physiological machinery is responsible for this?

■ What benefits does Charlie derive from this machinery?

The renin-angiotensin-aldosterone system can also work in the opposite direction: high salt intake, leading to high blood book and pressure, unremarkably inhibits renin secretion. With less angiotensin II formation and less aldosterone secretion, less table salt is retained past the kidneys and more is excreted in the urine. Unfortunately, many people with chronically high blood pressure may have normal or fifty-fifty elevated levels of renin secretion. In these cases, the intake of table salt must be lowered to friction match the dumb power to excrete common salt in the urine.

One °f the newer classes of drugs that can be used to treat hypertension (high claret force per unit area) are the __jTri angiotensin-converting enzyme, or ACE, inhibitors. These drugs (such every bit captopril) cake the germination of angiotensin 2, thus reducing its vasoconstrictor issue. The ACE inhibitors also increase the activity of bradykinin, a polypeptide that promotes vasodilation. The reduced formation of angiotensin II and increased action of bradykinin result in vasodila-tion, which decreases the total peripheral resistance. Because this reduces the afterload of the heart, the ACE inhibitors are also used to treat left ventricular hypertrophy and congestive heart failure. Another new class of antihypertensive drugs allows angiotensin 2 to exist formed but selectively blocks the angiotensin II receptors.

Atrial Natriuretic Peptide

As described in the previous section, a fall in blood book is compensated for past renal retentivity of fluid through activation of the renin-angiotensin-aldosterone organisation. An increase in blood volume, conversely, is compensated for past renal excretion of a larger book of urine. Experiments suggest that the increase in water excretion under weather of high claret volume is at least partly due to an increase in the excretion of Na+ in the urine, or natriuresis (natrium = sodium; uresis = making h2o).

Affiliate Xiv

Increased Na+ excretion (natriuresis) may exist produced by a decline in aldosterone secretion, but there is prove that in that location is a separate hormone that stimulates natriuresis. This natriuretic hormone would thus exist antagonistic to aldosterone and would promote Na+ and water excretion in the urine in response to a rising in blood volume. A polypeptide hormone with these properties, identified as atrial natriuretic peptide (ANP), is produced by the atria of the heart. By promoting salt and h2o excretion in the urine, ANP can human activity to lower the claret book and pressure. This is coordinating to the action of diuretic drugs taken by people with hypertension, as described later in this chapter.

In add-on to its stimulation of table salt and h2o excretion past the kidneys. ANP also antagonizes diverse actions of angiotensin II. As a event of this activeness, ANP decreases the secretion of aldosterone and promotes vasodilation.

Examination Yourself Before You lot Proceed

i. Depict the limerick of tissue (interstitial) fluid. Using a period diagram, explicate how tissue fluid is formed and how it is returned to the vascular system.

2. Define the term edema and describe iv different mechanisms that can produce this status.

3. Describe the effects of dehydration on blood and urine volumes. What crusade-and-result mechanism is involved?

4. Explicate why salt deprivation causes increased salt and water retention by the kidneys.

v. Describe the deportment of atrial natriuretic peptide and explain their significance.

Continue reading hither: Vascular Resistance to Claret Catamenia

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