{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,29]],"date-time":"2026-04-29T13:50:52Z","timestamp":1777470652790,"version":"3.51.4"},"reference-count":36,"publisher":"SAGE Publications","issue":"3","license":[{"start":{"date-parts":[[2013,7,16]],"date-time":"2013-07-16T00:00:00Z","timestamp":1373932800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Biological Research For Nursing"],"published-print":{"date-parts":[[2014,7]]},"abstract":"<jats:p>Blood pressure (BP) control is central to health promotion and maintenance across the health care continuum. Optimal control has been associated with improved microvascular end organ outcomes, reduced morbidity and mortality, and improved quality of life. Calcium channel blockers (CCBs) are a frequently utilized first-line antihypertensive agent, either as a monotherapy or in combination, as advocated by the 2003 Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC VII). However, despite their ability to achieve BP parameters comparable to alternative agents, CCBs may be inducing heart failure (HF) pathology by a mechanism other than the well-known negative inotropic effects of nondihydropyridine CCBs and thus may be responsible for more incident HF than was previously thought. Review of current literature indicates that there is a strong association between all types of CCBs and incident HF, that this association is found in persons with and without preexisting myocardial dysfunction, that BP measurement alone is an insufficient measure of end organ preservation with CCB use, and that CCB-induced HF is more problematic with comorbid coronary disease, renal disease, and diabetes mellitus. Furthermore, current research suggests that these outcomes are a result of CCB-induced neurohormonal sympathetic activation, sustained CCB-generated nitric oxide production leading to inflammation and tissue destruction, and\/or increased systemic calcification secondary to concurrent calcium supplementation. These findings suggest the pressing need for reevaluation of CCBs as first-line agents in treating hypertension and for possible revision of JNC VII hypertension guidelines.<\/jats:p>","DOI":"10.1177\/1099800413494760","type":"journal-article","created":{"date-parts":[[2013,7,17]],"date-time":"2013-07-17T20:14:06Z","timestamp":1374092046000},"page":"266-277","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":7,"title":["Calcium Channel Blockers as Initial Therapeutic Agents in Hypertension"],"prefix":"10.1177","volume":"16","author":[{"given":"Denise L.","family":"Shields","sequence":"first","affiliation":[{"name":"Virtua Health, Mt. 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