摘要:

This bibliography is produced in association withCurrent Opinion in Cardiology(Current Science Ltd, UK). Each issue of theJournal of Hypertensionlists papers relevant to hypertension, entered into the database over a specified period, arranged under subject headings. Papers may appear in more than one section. A complete, updated list of the journals scanned is included. A cumulative bibliography covering 12 months is published in the first issue (January) each year

ISSN:0263-6352    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

The presence of angiotensins was demonstrated in normal unstimulated alveolar macrophages and monocytes from both mice and rats. These peptides were partially purified from cell homogenates by ion exchange chromatography and identified as being [lle5] angiotensin I (Angl), [lle5] angiotensin II (Ang II) and to a lesser extent [lle4] angiotensin III (Ang III) using high performance liquid chromatography (HPLC). Based on the present data both alveolar macrophages and monocytes expressed Ang l as quantified by a specific and sensitive radio-immunoassay (RIA) from the HPLC eluates. In contrast to this, alveolar macrophages from both mice and rats exhibited a fairly low, if detectable Ang II content. It seems reasonable to suggest that, in contrast to monocytes, macrophages do not generate and/or incorporate Ang II appreciably, at least in their resting stageAlthough it is still not obvious whether these mononuclear phagocytes generate or simply capture angiolensin(s) from the blood pool or from the tissues; they must serve asin vivotarget cells for the angiotensin system, at least for the plasma or tissue clearance of these molecules

ISSN:0263-6352    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

In washed platelets both from DOCA-salt and renal hypertensive rats, there was a marked decrease in thrombin-induced aggregation and secretion responses compared with those of respective controls. Concomitantly, the platelets showed attentuated malondialdehyde (MDA) formation and reduced serotonin contents, suggesting the presence of degranulated platelets in the circulation due to hypertension. In platelets from stroke-prone spontaneously hypertensive rats (SHRSP) at early hypertensive stages, thrombin-induced aggregation and secretion responses were similarly reduced. However, the platelet hypofunctions did not accompany reduced MDA formation and serotonin contents. Properties of platelets obtained from SHRSP at late hypertensive stages resembled those of platelets from experimentally hypertensive rats. These results suggest that the mechanisms of platelet hypofunction differ between experimental hypertension and spontaneous hypertension in their early stages. The hypo-aggregability observed in experimental hypertension appears to be secondary to the hypertension, whereas that seen in spontaneous hypertension seems to be a primary defect and not secondary to hypertension at early stages of hypertension

ISSN:0263-6352    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

In patients with essential hypertension and healthy controls, plasma levels of atrial natriuretic peptide (ANP), angiotensin II (Ang II), aldosterone (Aldo), arginine vasopressin (AVP) and urinary excretion of prostaglandin E2(PGE2) were measured under basal conditions, and before and after acute volume expansion with a 2.5% hypertonic sodium chloride solution. Tubular sodium handling was assessed by the lithium clearance techniqueUnder basal conditions ANP was increased in patients compared with controls (9.0pmol/l versus 7.5pmol/l,P< 0.01). In response to acute volume expansion patients exhibited exaggerated increases in ANP (5.3pmol/l versus 3.0pmol/l,P< 0.05), exaggerated natriuresis, and an abnormal decrease in fractional proximal and distal tubular sodium reabsorption (PFRNaand DFRNa, respectively). Furthermore, during comparable urinary flow rates, urinary PGE2excretion was decreased in patients compared with controls (266pg/min versus 705pg/min,P< 0.05). No differences were found between patients and controls in Ang II, Aldo or AVP under basal conditions. Both groups responded to hypertonic acute volume expansion with comparable decreases in Ang II and Aldo, and an increase in AVPIt is concluded that in essential hypertension ANP is increased under basal conditions and the increase in natriuresis and ANP is exaggerated during acute volume expansion. The exaggerated natriuretic response to acute volume expansion resulted from an altered handling of sodium in both proximal and distal tubules

ISSN:0263-6352    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

Isolated tail arteries from stroke-prone spontaneously hypertensive rats (SHRSP), but not from normotensive Wistar-Kyoto rats (WKY), exhibit oscillatory contractions in response to norepinephrine. Previous studies indicate that the mechanism for these oscillations involves altered membrane calcium and/or potassium handling, and that this vascular change is a genetic defect associated with hypertension in SHRSP. The purpose of this experiment was to determine whether treatment of SHRSP with the calcium entry blocker felodipine would alter oscillatory activity. Adult SHRSP and WKY rats were treated orally with felodipine for 8 weeks. Felodipine treatment produced a significant decrease in blood pressure in SHRSP (control SHRSP: 240 ± 7 mmHg, n=6; felodipine-treated SHRSP: 164 ± 8 mmHg, n=5,P< 0.05; tail-cuff method). Helically-cut tail artery strips from all rats were mounted in tissue baths for isometric force recording and exposed to norepinephrine (6 x 10-9to 6 x 10-6mol/l) for 20min at each concentration. Oscillatory activity was defined as the sum of the magnitudes of all phasic contractions occurring during the final 10min of norepinephrine incubation. Oscillatory activity was markedly reduced in tail arteries from felodipine-treated SHRSP when compared with control SHRSP. Felodipine also inhibited oscillatory activity when added directly to the tissue bath. It seems, therefore, that felodipine may lower blood pressure in SHRSP, at least in part, by correcting the genetic defect responsible for oscillatory activity

ISSN:0263-6352    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

Thromboxane synthase is a cytochrome P-450-like enzyme requiring an iron-centered oxygen attack of the prostaglandin endoperoxide substrate (PGH2) for subsequent thromboxane A2(TxA2) formation. The activity and levels of P-450 enzymes can be manipulated by decreasing heme availability. Stannous chloride (SnCl2) selectively induces renal heme oxygenase activity, depleting heme and decreasing hemoprotein synthesis. We therefore manipulated the renal cytochrome P-450 system to influence thromboxane synthase activity, as measured by the conversion of14C-PGH2to thromboxane B2(TxB2) in renal cortical microsomes from spontaneously hypertensive rats (SHR). Seven-week-old SHR were treated subcutaneously with SnCl2(1, 10 and 15mg/100g body weight) for 4 consecutive days, and cortical microsomal heme oxygenase activity, heme content, P-450 content, thromboxane synthase activity and systolic blood pressure were measured. Heme oxygenase activity was significantly increased from 1058 ± 62nmol/mg protein in controls to 3125 ± 918, 5057 ± 690 —and 4236 ± 581 nmol/mg protein in SHR treated with 1,10 and 15mg/100g body weight SnCl2, respectively. The increase in heme oxygenase activity was associated with corresponding decreases in heme content (0.29 μmol/mg protein, for control to 0.12 μmol/mg protein for SHR treated with SnCl2, 10mg/100g body weight) and cytochrome P-450 content (0.18 ± 0.1 nmol/mg protein for control to 0.06 ± 0.01 nmol/mg protein for SHR treated with SnCl210mg/100g body weight). The reduction in heme and P-450 content was associated with a reduction in thromboxane synthase activity, i.e., decreases of 38, 35 and 47% from control levels at doses of 1, 10 and 15mg/100g body weight. Also, blood pressure was reduced dose-dependently with SnCl2treatment from 151 ± 3 (control) to 135 ± 3, 118 ± 2 and 114 ± 4 in SHR treated with SnCl2at doses of 1, 10 and 15mg/100g body weight, respectively. We conclude that it is possible to influence thromboxane synthase activity by affecting heme levels and thereby cytochrome P- 450 availability, and that the changes in thromboxane synthase activity may be important in the pathogenesis of hypertension in the SHR

ISSN:0263-6352    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

We compared the overflow of endogenous norepinephrine (NE) upon electrical stimulation, the associated pressor response and rate of initial neuronal uptake of3H-I-NE in the perfused mesenteric arteries of Dahl salt-sensitive (DS) and salt-resistant (DR) rats on two dietary NaCI regimens (0.4 and 8.0% for 2 weeks) from 4 weeks of age. The tissues of two rats, a DS and a DR control, were simultaneously processed and subjected to the same electrical stimulation. The pressor response and overflow of endogenous NE during periarterial nerve stimulation (5, 10 Hz, 1 min) in the tissue of DS rats on a high-salt diet (HS) were significantly greater, while those of DS on a low-salt diet (LS) were moderately but significantly higher than those of DR rats on either a high (HR) or a low-salt diet (LR). The tissue content of NE in DS rats was significantly lower than DR groups. There was a significantly reduced3H-I-NE uptake in the tissues of DS rats on both salt diet groups compared with DR rats. A submaximal dose of exogenous NE evoked a significantly greater pressor response amplitude in mesenteric tissues from DS rats on a high-salt diet than in any of the other three groups, suggesting that smooth muscle supersensitivity, either in the density of the NE receptor or in the excitation-contraction coupling system, had been induced in the vasculature of DS rats by feeding them on a high-salt diet for 2 weeks. These data indicate that enhanced NE overflow and smooth muscle supersensitivity to NE appear to be the most outstanding alterations induced in DS rats fed on a high-salt diet in the initial stages of hypertension

ISSN:0263-6352    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

Despite a high density ot atrial natriuretic factor (ANF) receptors, cultured vascular smooth muscle cells of the spontaneously hypertensive rat (SHR) manifest a blunted cyclic GMP (cGMP) response to ANF. We explored the role of cytosolic free Ca2++ ([Ca2+]¡) in the ANF-induced cGMP response of cultured aortic vascular smooth muscle cells from SHR and two normotensive rat strains: Wistar-Kyoto (WKY) and American Wistar. Exposure to 500nmol/l A23187 in Ca2+-containing but not in Ca2+-deficient medium resulted in a decline in the ANF-induced cGMP response at maximal ANF concentration (500nmol/l; SHR from 1004 ± 98 to 423 ±67,P< 0.001; WKY from 1791 ± 209 to 625 ±90,P< 0.001; American Wistar from 1496 ± 125 to 559 ± 96fmol/106cells/4min,P< 0.001). The same phenomenon was observed by depolarization with 50mmol/l KCI in Ca2 +-containing medium. There were no significant differences among the rat strains in basal levels of [Ca2 +]j. If Ca2+plays a role in the blunted cGMP response to ANF in vascular smooth muscle cells of the SHR, this effect may be exerted by a distinct pool of the ion in the submembrane domain which is associated with the particulate guanylate cyclase system

ISSN:0263-6352    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

Severe dietary sodium restriction initiated early in life is required to prevent development of hypertension in spontaneously hypertensive rats (SHR). Moderate sodium restriction does not affect hypertension development. This relative insensitivity to sodium restriction may be related to compensatory increases in other pressor mechanisms, specifically the renin-angiotensin system. We evaluated this possibility by measuring plasma renin activity, the blood pressure response to the angiotensin converting enzyme inhibitor captopril as well as blood pressure responsiveness to exogenous angiotensin II in SHR and Wistar-Kyoto rats (WKY) raised from birth until 6 or 16 weeks on control (101 µmol Na+/g food), moderate (26µmol/g) or two severe (17 or 9µmol/g) sodium-restricted diets. Moderate sodium restriction did not affect development of hypertension, but also did not cause significant increases in PRA or the blood pressure response to captopril in SHR or WKY. In contrast, severe sodium restriction blunted or prevented the development of hypertension in SHR and was associated with (1) marked increases in plasma renin activity (2) increased maintenance of blood pressure by the renin-angiotensin system (as assessed by captopril), and (3) a marked decrease in the blood pressure response to angiotensin II. We conclude that the relative insensitivity of hypertension development in SHR to dietary sodium restriction does not relate to a compensatory increase in the activity of the renin-angiotensin system. The moderate sodium restriction employed (26µmol/g) may rather represent the lower end of the normal range

ISSN:0263-6352    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

We assessed the relative contributions of raised cardiac output and increased peripheral resistance to elevation and lability of blood pressure in patients with borderline and sustained hypertension. Ninety-five untreated patients were admitted to hospital for assessment. Using Doppler ultrasound, linear cardiac output was measured as minute distance on the day of admission and 24 h later; blood pressure was measured at the same times, enabling calculation of linear resistance (analogous to peripheral vascular resistance). In sustained, but not borderline, hypertension linear resistance was increased at the first measurement (+ 36%,P< 0.001), but mean minute distance did not differ significantly from normal in either group. Between the first and second measurements in borderline and sustained hypertension there were significant falls of mean blood pressure (— 9%,P< 0.001 and - 4%,P< 0.01). In borderline, but not sustained, hypertension there was an associated fall of linear resistance (— 11%,P< 0.05); in neither group was there a significant change of minute distance. Both elevation and lability of blood pressure in borderline and sustained hypertension are due more to changes of peripheral resistance than to changes of cardiac output

ISSN:0263-6352    

出版商:OVID    

年代:1989

数据来源: OVID