Role of volume regulation in Resistant hypertension

What is the role of volume regulation in Resistant hypertension? How does it interfere with the efficacy of antihypertensive agents?

Volume overload from any underlying mechanism may not only increase the BP but may offset the effectiveness of antihypertensive drugs. Excessive salt intake and retention increases the plasma volume and causes resistance to antihypertensive drugs, and can actually raise the BP in some patients. Elderly and African American patients are particularly sensitive to fluid overload, as are patients with chronic kidney disease and congestive heart failure. Some antihypertensive drugs, such as direct vasodilators, antiadrenergic agents, and most of the non-diuretic antihypertensive drugs, cause plasma and extracellular fluid expansion, thus interfering with BP control. Of all the non-diuretic antihypertensive drugs, ACE inhibitors, angiotensin receptor blockers, and calcium antagonists are the least likely to cause fluid retention. Antihypertensive responsiveness can be regained by restricting the sodium intake; adding or increasing the dose of the diuretic; and, in some instances, switching to a loop diuretic from thiazides. In patients with advanced CKD, dialysis might be required for the adequate control of BP. Hypertension may be seemingly refractory if the antihypertensive drugs are used in suboptimal doses, or when an inappropriate diuretic is used (e.g., using a thiazide-type diuretic as opposed to a loop diuretic in patients with chronic kidney disease, congestive heart failure, and in those who are taking potent vasodilators, such as minoxidil or hydralazine). Inappropriate combinations can also limit their therapeutic potential. Adverse drug–drug interactions can raise the BP in patients with and without hypertension.

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