Publications
241 results found
Zhao L, Brown LA, Owji AA, et al., 1996, Adrenomedullin activity in chronically hypoxic rat lungs, American Journal of Physiology - Heart and Circulatory Physiology, Vol: 271, ISSN: 0363-6135
Adrenomedullin (AM) is a novel vasodilator with structural similarities to calcitonin gene-related peptide (CGRP). This study investigated AM activity in the rat lung during hypoxia-induced pulmonary hypertension. Both rat AM (0.2-10 nmol) and (α-CGRP (0.2-2 nmol) produced dose-related reductions in pulmonary artery pressure in the isolated perfused lung ventilated with 2% O2. Pretreatment with α-CGRP, which demonstrated tachyphylaxis, or its antagonist, CGRP-(8-37), reduced the hypotensive response to AM, suggesting that part of the response to AM is mediated by CGRP receptors. 125I-labeled AM and 125I-labeled CGRP binding was significantly increased in lung membranes from 7-day hypoxic animals (AM from 1.94 ± 0.3 to 3.36 ± 0.4 and CGRP from 0.06 ± 0.01 to 0.12 ± 0.02 pmol/mg protein), with no change in dissociation constant. Moreover, the hypotensive response to both peptides was increased in the lungs of 7-day hypoxic rats. There was no significant change in lung immunoreactive AM concentrations (hypoxic 5.04 ± 0.48 vs. control 6.28 ± 0.76 pmol/g wet wt of tissue) or steady-state AM mRNA levels in 7-day hypoxic rats. Nonetheless, AM may be useful for the acute pharmacological manipulation of pulmonary artery pressure in hypoxia-induced pulmonary hypertension.
Kirk JE, Wilkins, 1996, Renal effects of concurrent E-24.11 and ACE inhibition in the aortovenocaval fistula rat, Vol: 119, Pages: 943-948
BROWN LA, NUNEZ DJ, BROOKES CIO, et al., 1995, SELECTIVE INCREASE IN ENDOTHELIN-1 AND ENDOTHELIN-A RECEPTOR SUBTYPE IN THE HYPERTROPHIED MYOCARDIUM OF THE AORTO-VENACAVAL FISTULA RAT, CARDIOVASCULAR RESEARCH, Vol: 29, Pages: 768-774, ISSN: 0008-6363
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- Citations: 44
Brown LA, Nunez DJ, CIO B, et al., 1995, Selective increase in endothelin-1 and endothelin-A receptor subtype during cardiac hypertrophy in the rat, Cardiovascular Research, Vol: 29, Pages: 768-774
Good JM, Peters M, Wilkins MR, et al., 1995, Renal response to candoxatrilat in patients with heart failure, Journal of the American College of Cardiology, Vol: 25, Pages: 1273-1281
Hirokawa K, O'Shaughnessy KM, Ramrakha P, et al., 1994, Inhibition of nitric oxide synthase in vascular smooth muscle by retinoids, British Journal of Pharmacology, Vol: 113, Pages: 1448-1454
RUTHERFORD RAD, MATSUDA Y, WILKINS MR, et al., 1994, IDENTIFICATION OF RENAL NATRIURETIC PEPTIDE RECEPTOR SUBPOPULATIONS BY USE OF THE NONPEPTIDE ANTAGONIST, HS-142-1, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 113, Pages: 931-939, ISSN: 0007-1188
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- Citations: 12
RAD R, Matsuda Y, Wilkins MR, et al., 1994, Identification of renal natriuretic peptide receptor subpopulations by use of the non-peptide antagonist, HS-142-1, British Journal of Pharmacology, Vol: 113, Pages: 931-939
Hirokawa K, O'Shaughnessy K, Moore K, et al., 1994, Induction of nitric oxide synthase in cultured vascular smooth muscle cells: the role of cyclic AMP, British Journal of Pharmacology, Vol: 112, Pages: 396-402
Brown LA, Nunez DJ, Wilkins MR, 1993, Differential regulation of natriuretic peptide receptor mRNAs during the development of cardiac hypertrophy in the rat, Journal of Clinical Investigation, Vol: 92, Pages: 2702-2712
Kirk JE, Wilkins MR, 1993, Effect of endopeptidase-24.11 inhibition and atrial natriuretic peptide clearance receptor ligand on the response to rat brain natriuretic peptide in the conscious rat, British Journal of Pharmacology, Vol: 110, Pages: 350-354
CLESHAM GJ, KENNEDY A, LAVENDER JP, et al., 1993, METAIODOBENZYLGUANIDINE (METAIODOBENZYLGUANIDINE) SCANNING IN THE DIAGNOSIS OF PHEOCHROMOCYTOMA, JOURNAL OF HUMAN HYPERTENSION, Vol: 7, Pages: 353-356, ISSN: 0950-9240
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- Citations: 7
Clesham CJ, Kennedy A, Lavender JP, et al., 1993, Meta-iodobenzylguanidine (MIBG) scanning in the diagnosis of phaeochromocytoma, Journal of Human Hypertension, Vol: 7, Pages: 353-356
Wilkins MR, Nunez DJ, Wharton J, 1993, The natriuretic peptide family: turning hormones into drugs., J Endocrinol, Vol: 137, Pages: 347-359, ISSN: 0022-0795
Ligueros M, Unwin R, Wilkins MR, et al., 1992, A comparison of the effects of the selective peripheral alpha 1-blocker terazosin with the selective beta 1-blocker atenolol on blood pressure, exercise performance and the lipid profile in mild-to-moderate essential hypertension., Clin Auton Res, Vol: 2, Pages: 373-381, ISSN: 0959-9851
The effects of six weeks of treatment with the selective peripheral alpha 1-adrenoceptor blocker terazosin, or the selective beta 1-adrenoceptor blocker atenolol on blood pressure, exercise performance and blood lipid profile were compared in a single-blind, randomized, crossover study of 17 patients with mild-to-moderate essential hypertension. Although both drugs significantly reduced blood pressure at rest, atenolol caused a larger fall in supine blood pressure (11/11 and 7.5/7.0 mmHg, atenolol and terazosin, respectively; p < 0.001). Both treatments controlled the pressor response to exercise, although a greater reduction in diastolic blood pressure was observed at the end of exercise on terazosin (74.0 +/- 5.7 and 91.6 +/- 4.0 mmHg, terazosin and atenolol, respectively; p < 0.01). Alpha 1-blocker therapy was not associated with any measurable improvement or deterioration in cardiopulmonary performance and exercise duration. Unlike atenolol, terazosin therapy had the potentially beneficial effect of reducing serum total cholesterol levels and increasing the high-density lipoprotein-cholesterol/low-density lipoprotein-cholesterol ratio.
Ligueros M, Unwin RJ, Wilkins MR, et al., 1992, A comparison of the effects of the selective a-blocker terazosin with the selective b1-blocker atenolol on blood pressure control, serum lipids and exercise performance in mild-to-moderate hypertension, Clinical Autonomic Research, Vol: 2, Pages: 373-381
Wilkins MR, Settle SL, Kirk JE, et al., 1992, Response to atrial natriuretic peptide, endopeptidase-24.11 inhibition and C-ANP receptor ligand in the rat, British Journal of Pharmacology, Vol: 107, Pages: 50-57
WILKINS MR, NEEDLEMAN P, 1992, EFFECT OF PHARMACOLOGICAL MANIPULATION OF ENDOGENOUS ATRIOPEPTIN ACTIVITY ON RENAL-FUNCTION, AMERICAN JOURNAL OF PHYSIOLOGY, Vol: 262, Pages: F161-F167, ISSN: 0002-9513
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- Citations: 19
Wilkins MR, Needleman P, 1992, Effect of pharmacological manipulation of endogenous atriopeptin activity on renal function., Am J Physiol, Vol: 262, Pages: F161-F167, ISSN: 0002-9513
Atrial stretch causes the release of atriopeptin (AP, ANF) from preformed vesicular storage sites. The circulating hormone acts on unique receptor sites (containing guanylate cyclase) to release guanosine 3',5'-cyclic monophosphate (cGMP) that mediates the natriuresis and vasodilation and probably the suppression of renin, aldosterone, and vasopressin. The biological effects of atriopeptin are transient because of the rapid inactivation of the circulating hormone (by neutral endopeptidase or clearance receptors) or the second messenger (by cGMP-phosphodiesterase). Heart failure due to chronic cardiac volume overload [aortovenocaval (A-V) fistula] exhibits markedly elevated circulating AP blood levels and urinary cGMP levels, accompanied by induction of ventricular AP gene and protein expression and release. Pharmacological manipulation of endogenous AP, either by inhibiting cGMP phosphodiesterase (i.e., mediator prolongation) or neutral endopeptidase (i.e., prolongation of hormone half-life) in A-V fistula animals results in profound natriuresis and diuresis without hypotension. These pharmacological maneuvers bypass the suppressed renal response to exogenous AP seen in heart failure and provide a rational therapeutic strategy based on our understanding of the underlying physiological and pathological mechanisms.
Ligueros M, Unwin R, Wilkins M, 1991, Selective alpha 1-adrenoreceptor blockers in the treatment of hypertension: should we be using them more?, Clin Auton Res, Vol: 1, Pages: 251-258, ISSN: 0959-9851
It has become apparent in recent years that in the treatment of essential hypertension, reduction of blood pressure alone is not sufficient to reduce significantly the morbidity and mortality from ischaemic heart disease. Since the emergence of a multifactorial approach to the prevention of cardiovascular disease, the potential interaction between antihypertensive therapy and metabolic factors, such as control of blood glucose and lipid levels, has become an important consideration. Abnormal function of the sympathetic nervous system may contribute to both the initiation, or maintenance, of hypertension and the associated metabolic disturbances. The new generation of selective alpha 1-adrenoreceptor blockers, besides lowering blood pressure, appear to have favourable effects on lipid and glucose metabolism. The use of these drugs and their place in the treatment of hypertension are discussed.
Yan Q, Settle SL, Wilkins MR, 1991, Hypotension induced by intravascular administration of nerve growth factor in the rat, Clinical Science, Vol: 80, Pages: 565-569
GREENWALD JE, NEEDLEMAN P, WILKINS MR, et al., 1991, RENAL SYNTHESIS OF ATRIOPEPTIN-LIKE PROTEIN IN PHYSIOLOGY AND PATHOPHYSIOLOGY, AMERICAN JOURNAL OF PHYSIOLOGY, Vol: 260, Pages: F602-F607, ISSN: 0002-9513
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- Citations: 52
Greenwald JE, Needleman P, Wilkins MR, et al., 1991, Renal synthesis of atriopeptin-like protein in physiology and pathophysiology., Am J Physiol, Vol: 260, Pages: F602-F607, ISSN: 0002-9513
Atriopeptin is synthesized in mammalian atria as a 126-amino acid (14 kDa) prohormone, but it is secreted and circulates as a 28-amino acid (2.5 kDa) peptide. We have demonstrated the synthesis and secretion of an atriopeptin-like peptide in neonatal and adult rat kidney cell cultures. In this study, we evaluated the site of renal synthesis of this protein and its expression in normal rats and rats made nephrotic with puromycin aminonucleoside. The major form of atriopeptin in normal kidneys comigrated with an apparent molecular mass of 2.5 kDa assessed by gel filtration chromatography. However, the major form of this atriopeptin-like protein in nephrotic kidneys was determined to have an apparent molecular mass similar to the heart prohormone. No atriopeptin prohormone was detected in the plasma of nephrotic rats. Localization of this renal atriopeptin-like protein was accomplished by immunocytochemistry of rat kidney frozen sections. Using an antibody generated against either the COOH-terminal or NH3-terminal region of the cardiac atriopeptin prohormone, we detected specific immunostaining in the distal cortical nephron of the nephrotic kidney. This is the first report of the anatomic localization of a renal atriopeptin-like protein and its upregulation in nephrosis.
Greenwald JE, Needleman P, Wilkins MR, et al., 1991, Renal atriopeptin synthesis in rats in physiology and pathophysiology, American Journal of Physiology, Vol: 260, Pages: 602-607
Toki Y, Ito T, Shiono S, et al., 1990, Alternative mechanisms for atriopeptin prohormone processing by isolated perfused rat hearts, Journal of Pharmacology & Experimental Therapeutics, Vol: 254, Pages: 228-235
Wilkins MR, Settle SL, Needleman P, 1990, Augmentation of the natriuretic activity of exogenous and endogenous atriopeptin in rats by inhibition of guanosine 3', 5'-cyclic GMP monophosphate degradation, Journal of Clinical Investigation, Vol: 85, Pages: 1274-1279
Wilkins MR, Settle SL, Stockmann PT, et al., 1990, Maximizing the natriuretic effect of endogenous atriopeptin in a rat model of heart failure, Proceedings of the National Academy of Sciences USA, Vol: 87, Pages: 6465-6469
LEWIS HM, WILKINS MR, KENDALL MJ, et al., 1989, CARBIDOPA DOES NOT AFFECT THE RENAL RESPONSE TO ATRIAL NATRIURETIC FACTOR IN MAN, CLINICAL SCIENCE, Vol: 77, Pages: 281-285, ISSN: 0143-5221
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- Citations: 8
WILKINS MR, STOTT RAW, LEWIS HM, 1989, ATRIAL NATRIURETIC FACTOR, ANNALS OF CLINICAL BIOCHEMISTRY, Vol: 26, Pages: 115-118, ISSN: 0004-5632
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- Citations: 5
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