Comparison of 24‐Hour Ambulatory Blood Pressure Data in Hypertensive Patients Switched from Nifedipine‐GITS to Nifedipine‐CC

Wurdeman, Richard L.; Mooss, Aryan N.; Mohiuddin, Syed M.; Lucas, B. Daniel; Ryschon, Kay; Hilleman, Daniel E.

doi:10.1592/phco.19.1.94.30512

Cited by 5 publications

(4 citation statements)

References 11 publications

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“…There have been inconsistent findings when switching from one dihydropyridine CCB to another or when switching to different formulations of the same drug to lessen or resolve peripheral edema 29–31 . Edema will diminish upon conversion from a dihydropyridine CCB to a nondihydropyridine CCB such as verapamil or diltiazem.…”

Section: Treatment Of Ccb‐related Edemamentioning

confidence: 99%

Calcium Channel Blocker‐Related Peripheral Edema: Can It Be Resolved?

Sica

2003

J of Clinical Hypertension

120

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Calcium channel blocker (CCB)-related edema is quite common in clinical practice and can effectively deter a clinician from continued prescription of these drugs. Its etiology relates to a decrease in arteriolar resistance that goes unmatched in the venous circulation. This disproportionate change in resistance increases hydrostatic pressures in the precapillary circulation and permits fluid shifts into the interstitial compartment. CCB-related edema is more common in women and relates to upright posture, age, and the choice and dose of the CCB. Once present it can be slow to resolve without intervention. A number of strategies exist to treat CCB-related edema, including switching CCB classes, reducing the dosage, and/or adding a known venodilator such as a nitrate, an angiotensin-converting enzyme inhibitor, or an angiotensin-receptor blocker to the treatment regimen. Angiotensin-converting enzyme inhibitors have been best studied in this regard. Diuretics may alter the edema state somewhat, but at the expense of further reducing plasma volume. Traditional measures such as limiting the amount of time that a patient is upright and/or considering use of graduated compression stockings are useful adjunctive therapies. Discontinuing the CCB and switching to an alternative antihypertensive therapy will resolve the edema.

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Section: Treatment Of Ccb‐related Edemamentioning

confidence: 99%

Calcium Channel Blocker‐Related Peripheral Edema: Can It Be Resolved?

Sica

2003

J of Clinical Hypertension

120

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“…An additional option in certain instances (where the glomerular filtration rate decrease is not excessive) is to consider CCB therapy together with an ACE inhibitor (or ARB). [160][161][162] Resolution of peripheral edema by drug switching (at least with the older CCBs) is unlikely to reflect fundamental biologic differences between drugs. 158 The chronic use of CCBs has also been shown to be a cause of bilateral symmetric false-positive captopril renography in patients with established renal artery stenosis.…”

Section: Ccb Overdosementioning

confidence: 99%

“…Among the several dihydropyridine CCBs, there have been inconsistent findings when switching from one dihydropyridine CCB to another or when converting to different formulations of the same drug to lessen or resolve the peripheral edema. [160][161][162] Resolution of peripheral edema by drug switching (at least with the older CCBs) is unlikely to reflect fundamental biologic differences between drugs. 162 If there is a relevant difference in the biology of these compounds, it would have to be ascribed to differences in vascular permeability and/or differing effects on precapillary and postcapillary vascular resistance.…”

Section: Chronopharmacologymentioning

confidence: 99%

Pharmacologic and Therapeutic Considerations in Hypertension Therapy With Calcium Channel Blockers: Focus on Verapamil

Sica

Prisant

2007

J of Clinical Hypertension

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In the past 2 decades, calcium channel blockers have emerged as important and useful agents for treating hypertension. The safety of this drug class has been vigorously debated for some time, and it has only been in the past few years that such debate has been quieted by favorable outcomes data with these compounds. Calcium channel blockers are a heterogeneous group of compounds as alike as they are dissimilar. Calcium channel blockers can be separated into dihydropyridine and nondihydropyridine subclasses, with representatives of the latter being verapamil and diltiazem. A lengthy treatment experience exists for verapamil, a compound that has progressed from an immediate‐release to a sustained‐release and, more recently, a delayed/sustained‐release formulation designated for administration at bedtime. This latter formulation synchronizes drug delivery with the early morning rise in blood pressure, which is a particularly attractive feature when viewed in the context of the distinctive pharmacokinetic and pharmacodynamic features of verapamil.

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“…In animal models, proliferation and migration of VSMC begin soon after vascular injury occurs and culminate in formation of a neointima that encroaches on the interior space of the vessel (1). Such neointima formation is seen in a substantial number of patients following balloon angioplasty and may result in a narrowing or blockage (restenosis) of the vessel that requires further intervention (2). By preventing the immediate proliferation of VSMC following vascular injury, it may be possible to avert neointima formation and restenosis.…”

Section: Although Vascular Smooth Muscle Cells (Vsmc)mentioning

confidence: 99%

An Exochelin of Mycobacterium tuberculosis Reversibly Arrests Growth of Human Vascular Smooth Muscle Cells in Vitro

Pahl¹,

Yan²,

Hodges³

et al. 2000

Journal of Biological Chemistry

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Proliferation of vascular smooth muscle cells (VSMC)is characteristic of restenosis following balloon angioplasty. We show here that a low concentration of a novel iron chelator, desferri-exochelin 772SM, reversibly arrests the growth of human VSMC in vitro, specifically in G 0 /G 1 and S phases. The lipophilic desferri-exochelin is effective more rapidly and at a 10-fold lower concentration than the nonlipophilic iron chelator deferoxamine. Treatment of growth-synchronized VSMC with the desferri-exochelin results in down-regulation of cyclin E/ Cdk2 and cyclin A/Cdk2 activity but does not affect the cyclin D/Cdk4/retinoblastoma phosphorylation pathway. Both DNA replication and RNA transcription are inhibited in exochelin-treated cells, but protein synthesis is not. The ability of desferri-exochelin 772SM to reversibly block the growth of VSMC in vitro with no apparent cytotoxicity suggests that the exochelin may be useful as a therapeutic agent to limit restenosis in injured vessels.Although vascular smooth muscle cells (VSMC) 1 are normally quiescent, they enter the cell cycle when exposed to growth factors in vitro or following vascular injury in vivo. In animal models, proliferation and migration of VSMC begin soon after vascular injury occurs and culminate in formation of a neointima that encroaches on the interior space of the vessel (1). Such neointima formation is seen in a substantial number of patients following balloon angioplasty and may result in a narrowing or blockage (restenosis) of the vessel that requires further intervention (2). By preventing the immediate proliferation of VSMC following vascular injury, it may be possible to avert neointima formation and restenosis. In this report, we describe the cell cycle-specific growth inhibitory effects of a novel iron chelator, desferri-exochelin 772SM, on serum-and growth factor-stimulated human VSMC in vitro.Iron is required for a variety of cellular functions, including respiration, energy metabolism, and DNA synthesis. In addition, iron participates in redox reactions that generate free radicals, which may activate signaling pathways for cell proliferation. Treatment with iron chelators has previously been shown to cause growth arrest in several types of cells (3-5). However, the effect of chelation varied depending upon both the cell type and the chelator used (5-7).The iron chelator deferoxamine (DFO) inhibited DNA synthesis in cultured rat VSMC (8) and blocked neointimal growth in a rat model of vascular injury (8). However, DFO enters cells only very slowly by pinocytosis (9) and causes hypotension when given in large doses in vivo (10). Therefore, DFO is of limited usefulness for determining mechanisms by which iron deprivation prevents cell cycle progression or for the clinical treatment of restenosis.Exochelins, the secreted siderophores of Mycobacterium tuberculosis, are a family of high affinity iron chelators that are both water-and lipid-soluble, a property that allows them to enter cells rapidly and chelate specific intracellular iro...

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Comparison of 24‐Hour Ambulatory Blood Pressure Data in Hypertensive Patients Switched from Nifedipine‐GITS to Nifedipine‐CC

Cited by 5 publications

References 11 publications

Calcium Channel Blocker‐Related Peripheral Edema: Can It Be Resolved?

Calcium Channel Blocker‐Related Peripheral Edema: Can It Be Resolved?

Pharmacologic and Therapeutic Considerations in Hypertension Therapy With Calcium Channel Blockers: Focus on Verapamil

An Exochelin of Mycobacterium tuberculosis Reversibly Arrests Growth of Human Vascular Smooth Muscle Cells in Vitro

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