Sympathetic Nervous System

The nervous system, which reacts within seconds after a drop in BP, increases BP primarily by activating the SNS. Increased SNS activity increases HR and cardiac contractility, produces widespread vasoconstriction in the peripheral arterioles, and promotes the release of renin from the kidneys. The net effect of SNS activation is to increase BP by increasing both CO and SVR.

Specialized nerve cells called baroreceptors (pressoreceptors) are located in the carotid arteries and the arch of the aorta. These cells sense changes in BP and transmit this information to the vasomotor centers in the brainstem. The brainstem sends this information through complex networks of neurons that excite or inhibit efferent nerves. SNS efferent nerves innervate cardiac and vascular smooth muscle cells. Under normal conditions, a low level of continuous SNS activity maintains vascular tone. BP may be reduced by withdrawal of SNS activity or by stimulation of the parasympathetic nervous system. This decreases the HR (via the vagus nerve) and thereby decreases CO.

The neurotransmitter norepinephrine (NE) is released from SNS nerve endings. NE activates receptors located in the sinoatrial node, myocardium, and vascular smooth muscle. The response to NE depends on the type of receptors present. SNS receptors are classified as α₁, α₂, β₁, and β₂ (Table 33-1). The smooth muscle of the blood vessels has α-adrenergic and β₂-adrenergic receptors. α-Adrenergic receptors located in the peripheral vasculature cause vasoconstriction when stimulated by NE. β₁-Adrenergic receptors in the heart respond to NE and epinephrine with increased HR (chronotropic), increased force of contraction (inotropic), and increased speed of conduction (dromotropic). β₂-Adrenergic receptors are activated primarily by epinephrine released from the adrenal medulla and cause vasodilation (see Fig. 33-1).

The sympathetic vasomotor center interacts with many areas of the brain to maintain normal BP under various conditions. It is activated during times of pain, stress, and exercise. The SNS response causes an appropriate increase in CO and BP to adjust to the body’s increased oxygen demands. During postural change from lying to standing, there is a transient decrease in BP. The vasomotor center is stimulated, and the SNS response causes peripheral vasoconstriction and increased venous return to the heart. If this response did not occur, blood flow to the brain would be inadequate, resulting in dizziness or syncope.

Vascular Endothelium

The vascular endothelium is a single-cell layer that lines the blood vessels. It produces several vasoactive substances and growth factors. Nitric oxide and prostacyclin help maintain low arterial tone, inhibit growth of the smooth muscle layer, and inhibit platelet aggregation. Endothelin (ET) is an extremely potent vasoconstrictor. It also causes adhesion and aggregation of neutrophils and stimulates smooth muscle growth (see Fig. 33-1).

Renal System

The kidneys contribute to BP regulation by controlling sodium excretion and extracellular fluid (ECF) volume (see Chapter 45). Sodium retention results in water retention, which causes an increased ECF volume. This increases the venous return to the heart and the stroke volume. Together, these increase CO and BP.

The renin-angiotensin-aldosterone system (RAAS) also plays an important role in BP regulation (see Fig. 33-1). The juxtaglomerular apparatus in the kidney secretes renin in response to SNS stimulation, decreased blood flow through the kidneys, or decreased serum sodium concentration. Renin is an enzyme that converts angiotensinogen to angiotensin I. Angiotensin-converting enzyme (ACE) converts angiotensin I into angiotensin II (A-II). A-II increases BP by two different mechanisms (see Fig. 45-4). First, A-II is a potent vasoconstrictor and increases SVR. This results in an immediate increase in BP. Second, over a period of hours or days, A-II increases BP indirectly by stimulating the adrenal cortex to secrete aldosterone (discussed below).

A-II also acts at a local level within the heart and blood vessels. These effects include vasoconstriction and tissue growth that results in remodeling of the vessel walls. These changes are linked to the development of primary hypertension and also the long-term effects of hypertension (e.g., atherosclerosis, renal disease, cardiac hypertrophy).

Prostaglandins (PGE₂ and PGI₂) secreted by the renal medulla have a vasodilator effect on the systemic circulation. This results in decreased SVR and lowering of BP. (Prostaglandins are discussed in Chapter 12.) The natriuretic peptides (atrial natriuretic peptide [ANP] and b-type natriuretic peptide [BNP]) are secreted by heart cells. They antagonize the effects of antidiuretic hormone (ADH) and aldosterone. This results in natriuresis (excretion of sodium in urine) and diuresis, resulting in reduced blood volume and BP.

Endocrine System

Stimulation of the SNS results in release of epinephrine along with a small fraction of NE by the adrenal medulla. Epinephrine increases the CO by increasing the HR and myocardial contractility. Epinephrine activates β₂-adrenergic receptors in peripheral arterioles of skeletal muscle, causing vasodilation. In peripheral arterioles with only α₁-adrenergic receptors (skin and kidneys), epinephrine causes vasoconstriction.

A-II stimulates the adrenal cortex to release aldosterone. (Release of aldosterone is also regulated by other factors [see Chapters 48 and 50].) Aldosterone stimulates the kidneys to retain sodium and water. This increases blood volume and CO (see Fig. 45-4).

An increased blood sodium and osmolarity level stimulates the release of ADH from the posterior pituitary gland. ADH increases the ECF volume by promoting the reabsorption of water in the distal and collecting tubules of the kidneys. The resulting increase in blood volume causes an increase in CO and BP.

Etiology

Hypertension can be classified as either primary or secondary.

Pathophysiology of Primary Hypertension

BP rises with any increase in CO or SVR. Increased CO is sometimes found in the person with prehypertension. Later in the course of hypertension, the SVR rises and the CO returns to normal. The hemodynamic hallmark of hypertension is persistently increased SVR. This persistent elevation in SVR may occur in various ways. Table 33-4 presents factors that relate to the development of primary hypertension or contribute to its consequences. Abnormalities of any of the mechanisms involved in the maintenance of normal BP can result in hypertension (see Fig. 33-1).

 Genetic Link

Different sets of genes may regulate BP at different times throughout the life span.² Genetic abnormalities associated with a rare form of hypertension characterized by excess levels of potassium have been identified. To date, the known contribution of genetic factors to BP in the general population remains very small.¹

The International Consortium for Blood Pressure Genome-Wide Association Studies is a network of researchers currently working to uncover genetic factors related to hypertension. In practice, you should screen children and siblings of persons with hypertension and strongly advise them to adopt healthy lifestyles to prevent hypertension.

Clinical Manifestations

Hypertension is often called the “silent killer” because it is frequently asymptomatic until it becomes severe and target organ disease occurs. A patient with severe hypertension may experience a variety of symptoms secondary to the effects on blood vessels in the various organs and tissues or to the increased workload of the heart. These secondary symptoms include fatigue, dizziness, palpitations, angina, and dyspnea. In the past, symptoms of hypertension were thought to include headache and nosebleeds. Unless BP is very high, these symptoms are no more frequent in people with hypertension than in the general population. However, patients with hypertensive crisis (discussed later in the chapter) may experience severe headaches, dyspnea, anxiety, and nosebleeds.¹¹

Complications

The most common complications of hypertension are target organ diseases occurring in the heart (hypertensive heart disease), brain (cerebrovascular disease), peripheral vessels (peripheral vascular disease), kidneys (nephrosclerosis), and eyes (retinal damage) (Table 33-5).

TABLE 33-5

MANIFESTATIONS OF TARGET ORGAN DISEASE

Organ	Manifestations
Cardiac	• Clinical, electrocardiographic, or radiologic evidence of coronary artery disease (e.g., previous myocardial infarction, coronary revascularization) • Left ventricular hypertrophy by ECG or echocardiography • Left ventricular dysfunction or heart failure
Cerebrovascular	• Transient ischemic attack • Stroke
Peripheral vascular	• One or more major pulses in the extremities (except for dorsalis pedis) reduced or absent • Intermittent claudication • Abdominal or carotid bruits or thrills • Aneurysm Only gold members can continue reading. Log In or Register to continue Share this: Click to share on Twitter (Opens in new window) Click to share on Facebook (Opens in new window) Related Related posts: Introduction Nursing Management: Sexually Transmitted Infections Nursing Assessment: Cardiovascular System Nursing Management: Musculoskeletal Problems Stay updated, free articles. Join our Telegram channel Join Tags: Medical-Surgical Nursing Assessment and Management of Clinical P Nov 17, 2016 | Posted by admin in NURSING | Comments Off on Nursing Management: Hypertension Full access? Get Clinical Tree Get Clinical Tree app for offline access Get Clinical Tree app for offline access