184 results found
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
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
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
BROWN LA, NUNEZ DJR, WILKINS MR, 1993, DIFFERENTIAL REGULATION OF NATRIURETIC PEPTIDE RECEPTOR MESSENGER-RNAS DURING THE DEVELOPMENT OF CARDIAC-HYPERTROPHY IN THE RAT, JOURNAL OF CLINICAL INVESTIGATION, Vol: 92, Pages: 2702-2712, ISSN: 0021-9738
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
Clesham CJ, Kennedy A, Lavender JP, et al., 1993, Meta-iodobenzylguanidine (MIBG) scanning in the diagnosis of phaeochromocytoma., J Hum Hypertens, Vol: 7, Pages: 353-356, ISSN: 0950-9240
During the period 1984-90, meta-iodobenzylguanidine (MIBG) scans were performed in 23 patients with suspected phaeochromocytoma seen at the Hammersmith Hospital. Sixteen patients had a histologically proven phaeochromocytoma and in 14 of these patients the tumour was demonstrated by abnormal uptake of MIBG. Seven patients did not have a phaeochromocytoma and in all of these the MIBG scan was negative. These findings gave the procedure a sensitivity of 87.5% with a specificity of 100%; positive and negative predictive values were 100% and 77.7%, respectively. MIBG scanning is an extremely valuable technique in the management of patients with suspected phaeochromocytoma but is best employed to localise a tumour which has been confirmed biochemically.
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
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, 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
WILKINS MR, SETTLE SL, KIRK JE, et al., 1992, RESPONSE TO ATRIAL NATURIURETIC PEPTIDE, ENDOPEPTIDASE 24.11 INHIBITOR AND C-ANP RECEPTOR LIGAND IN THE RAT, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 107, Pages: 50-57, ISSN: 0007-1188
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.
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
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
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.
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, ISSN: 0143-5221
GREENWALD JE, NEEDLEMAN P, WILKINS M, et al., 1990, RENAL SYNTHESIS OF ATRIOPEPTIN IN PHYSIOLOGY AND PATHO-PHYSIOLOGY, Publisher: BLACKWELL SCIENCE INC, Pages: 339-339, ISSN: 0085-2538
TOKI Y, ITO T, SHIONO S, et al., 1990, ALTERNATIVE MECHANISMS FOR ATRIOPEPTIN PROHORMONE PROCESSING BY ISOLATED PERFUSED RAT HEARTS, JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS, Vol: 254, Pages: 228-235, ISSN: 0022-3565
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-MONOPHOSPHATE DEGRADATION, JOURNAL OF CLINICAL INVESTIGATION, Vol: 85, Pages: 1274-1279, ISSN: 0021-9738
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 OF THE UNITED STATES OF AMERICA, Vol: 87, Pages: 6465-6469, ISSN: 0027-8424
LEWIS HM, RATCLIFFE WA, STOTT RAW, et al., 1989, DEVELOPMENT AND VALIDATION OF A 2-SITE IMMUNORADIOMETRIC ASSAY FOR HUMAN ATRIAL NATRIURETIC FACTOR IN UNEXTRACTED PLASMA, CLINICAL CHEMISTRY, Vol: 35, Pages: 953-957, ISSN: 0009-9147
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
Lewis H, Wilkins M, Selwyn B, et al., 1989, Relationship between ANP, cyclic GMP and tissue kallikrein following saline infusion in healthy volunteers., Adv Exp Med Biol, Vol: 247A, Pages: 281-286, ISSN: 0065-2598
Infusion of saline in healthy volunteers produced a significant rise in plasma atrial natriuretic peptide, which was accompanied by the urinary excretion of cyclic GMP and sodium. Although the time-course of cyclic GMP excretion almost mirrored that of plasma ANP, that of sodium showed sustained phase, indicating involvement of additional humoral regulators. ANP did not stimulate the excretion of enzymic or immunoreactive tissue kallikrein.
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: 73, Pages: 281-285
WILKINS MR, STOTT RAW, LEWIS HM, 1989, ATRIAL NATRIURETIC FACTOR, ANNALS OF CLINICAL BIOCHEMISTRY, Vol: 26, Pages: 115-118, ISSN: 0004-5632
LEWIS HM, WILKINS MR, SELWYN BM, et al., 1988, URINARY GUANOSINE 3'-5'-CYCLIC MONOPHOSPHATE BUT NOT TISSUE KALLIKREIN FOLLOWS THE PLASMA ATRIAL NATRIURETIC FACTOR RESPONSE TO ACUTE VOLUME EXPANSION WITH SALINE, CLINICAL SCIENCE, Vol: 75, Pages: 489-494, ISSN: 0143-5221
WILKINS MR, GAMMAGE MD, LEWIS HM, et al., 1988, EFFECT OF LOWER BODY POSITIVE PRESSURE ON BLOOD-PRESSURE, PLASMA ATRIAL NATRIURETIC FACTOR CONCENTRATION, AND SODIUM AND WATER-EXCRETION IN HEALTHY-VOLUNTEERS AND CARDIAC TRANSPLANT RECIPIENTS, CARDIOVASCULAR RESEARCH, Vol: 22, Pages: 231-235, ISSN: 0008-6363
BEERAHEE M, WILKINS MR, JACK DB, et al., 1987, 12 HOUR (TROUGH) PLASMA NIFEDIPINE CONCENTRATIONS DURING CHRONIC TREATMENT WITH NIFEDIPINE-RETARD, EUROPEAN JOURNAL OF CLINICAL PHARMACOLOGY, Vol: 32, Pages: 347-349, ISSN: 0031-6970
Beerahee M, Wilkins MR, Jack DB, et al., 1987, Twelve hour (tough) plasma nifedipine concentrations during chronic treatment with nifedipine retard, European Journal of Clinical Pharmacology, Vol: 32, Pages: 347-349
This data is extracted from the Web of Science and reproduced under a licence from Thomson Reuters. You may not copy or re-distribute this data in whole or in part without the written consent of the Science business of Thomson Reuters.