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B H Swords

Publications and source records attributed to B H Swords.

7 recordsLinked to original sources
PubMed1992

Effect of angiotensin converting enzyme inhibitors upon brain angiotensin II binding.

OBJECTIVE: The major objective of the current study was to determine whether administration of converting enzyme (CEI) inhibitors produces an alteration in angiotensin II receptor binding in the spontaneously hypertensive rat (SHR). DESIGN: These studies were designed to test the hypothesis that administration of CEI to SHR is associated with a downregulation of the brain angiotensin II receptor. METHODS: Ten to fifteen rats per group were used as mating pairs to produce the pups used for cell culture. The specific binding of 125I-angiotensin II to cell membranes was determined in primary neuronal enriched cultures (PNC) developed from whole brains of 1-day-old SHR pups treated in utero with captopril compared with control SHR pups. We then determined the effect of short-term incubation of PNC with captopril or lisinopril upon angiotensin II binding kinetics. RESULTS: 125I-angiotensin II binding in PNC from captopril-treated SHR was decreased compared with cells from control rats. Scatchard analysis revealed no differences in receptor affinity but maximum density of binding sites was less in captopril-treated rats than in controls. Short-term incubation of cells with captopril or lisinopril did not affect angiotensin II binding in neuronal cultures from normotensive rats; however, angiotensin II binding was decreased in SHR cells treated with captopril. Angiotensin II binding was also decreased in SHR treated in utero with captopril. CONCLUSIONS: These data suggest that CEI decrease 125I-angiotensin II binding in brains from SHR and, furthermore, that the angiotensin II receptor in SHR may be regulated differently from that of normotensive rats.

Angiotensin II↗
PubMed1991

Central vasopressin receptors are upregulated by deoxycorticosterone acetate.

Studies were performed to characterize the regulation of central vasopressin (AVP) receptors in deoxycorticosterone acetate (DOCA)-NaCl-treated and control rats, and in DOCA-treated primary neuronal enriched cell cultures. Uninephrectomized rats were given NaCl to drink and implanted subcutaneously with a silastic implant containing 200 mg/kg DOCA. [3H]AVP binding to a diencephalic block of tissue was examined. Whereas DOCA-NaCl treatment did not affect the affinity of [3H]AVP binding, the total number of AVP receptors was increased between 3 and 14 days following DOCA-NaCl administration. No differences in the number of binding sites were present in the established (35-56 days after DOCA-NaCl administration) stages of hypertension. To determine whether the increase in [3H]AVP binding was a direct effect of DOCA on neurons or related to the hormonal, volume or other physiologic changes that DOCA-NaCl treatment causes in the whole animal, [3H]AVP binding was examined in neurons grown in culture that was treated with DOCA. Scatchard analysis demonstrated that DOCA treatment (compared to control) produced an increase in the number but no change in the affinity of the AVP binding sites in primary neuron-enriched cultures. Treatment of cultured neurons with other steroids (estrogen, corticosterone, or aldosterone), did not change the kinetics of [3H]AVP binding, suggesting that the effects of DOCA on the AVP receptor were specific for this steroid. These data indicate that, in comparison to control rats, DOCA-NaCl hypertensive rats, have an enhanced number of AVP receptors in the diencephalon, perhaps as a direct result of an interaction between DOCA and AVP receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Alterations in vasopressin mechanisms in captopril-treated spontaneously hypertensive rats.

The effects of lifetime captopril treatment on vasopressin (VP) were assessed in spontaneously hypertensive rats (SHR). Pregnant and nursing dams were treated with oral Captopril (100 mg/kg/day). After weaning, the pups were maintained on Captopril (50/kg/day) for 19-20 wks. Blood pressures of Captopril-treated SHR were in the normotensive range and significantly lower (p less than .001) than SHR control rats. Control and Captopril-treated SHR were perfused and brains were sectioned for immunohistochemical staining with a polyclonal antibody directed against vasopressin (VP). Compared to control SHR, Captopril-treated rats displayed decreased VP-like immunoreactivity in the paraventricular (PVN) and supraoptic (SON) nuclei of the hypothalamus. Captopril treatment also selectively decreased the number of brightly labeled cell bodies in the SON and PVN and reduced VP-like labeling in the axons of the neurons in these nuclei. Concurrent with a decrease in VP-like immunoreactivity, Captopril treatment reduced plasma VP levels (RIA) (p less than 0.01, Captopril, 5.6 +/- 0.5 pg/ml; control, 11.8 +/- 2.2 pg/ml). Scatchard analysis of 3H-VP binding indicated that Captopril treatment increased the number but not the affinity of VP receptors in the hypothalamus and brain stem of SHR. These results suggest that in SHR oral Captopril treatment attenuates the synthesis and release of VP, an effect that may contribute to the blood pressure lowering effect of converting enzyme inhibitors.

Animals↗
PubMed1991

Cloning and direct sequencing from lambda cDNA libraries using the polymerase chain reaction: suppressin and the vasopressin receptor as models.

A strategy using the polymerase chain reaction (PCR) to screen a lambda gt11 pituitary cDNA library for cDNAs encoding suppressin, a putative anti-proliferative protein, and a putative vasopressin receptor is described. The use of this technique will facilitate the demonstration of e.g. the presence of "neuropeptide receptors" on cells of the lymphoid system, confirming the concept of "shared ligands and receptors" by the neuroendocrine and the immune system. Neither of the genes encoding the proteins of the present study have previously been cloned. The PCR-screening procedure requires sequence information from the gene of interest which permits the generation of complementary primers. These primers are then used in combination with lambda phage primers complementary to regions flanking the cloning site in a PCR to amplify cDNAs derived from the gene of interest. This novel screening procedure yields cDNA related to the gene of interest, including the largest clone present in the library. To confirm the utility of this technique for cDNA libraries, the library was also screened using traditional cDNA hybridization techniques. The largest clone obtained by screening the cDNA library with PCR was the same as that obtained by the conventional technique. Thus, the results of these studies show that the PCR method can be used instead of more conventional means to screen cDNA libraries. Lastly, we describe a protocol for directly sequencing PCR-amplified DNA using the same primers that are used for amplification. The combined use of these two strategies permits cloning and sequencing of cDNAs from lambda cDNA libraries in a fraction of the time required using traditional screening techniques, but with identical results.

Animals↗
PubMed1990

An antibody directed against a peptide encoded by RNA complementary to mRNA for vasopressin recognizes putative vasopressin receptors.

The purpose of this study was to generate an antibody against the binding site of the vasopressin receptor. Recently it has been demonstrated that complementary RNA sequences may encode interacting peptides. We determined whether or not an antibody directed against a peptide (PVA) specified by RNA complementary to the mRNA of rat arginine vasopressin (AVP) would recognize the AVP receptor. The antibody was purified sequentially over a protein A and then a PVA affinity column. A specific anti-PVA antibody affinity column also was made. The specific anti-PVA antibody recognized two proteins with molecular weights of 76 and 70 kD in homogenates from kidney and brain tissue containing the hypothalamus/thalamus/septum. This antibody also blocked binding of 3H-AVP to primary cultured neuronal cells, whereas the nonspecific antibody did not. Furthermore, the blocking efficiency of the antibody increased when more of the specific anti-PVA antibody was present. We also determined whether or not the antiserum contained any biological activity by observing urine volume and urine osmolality in the presence or absence of preimmune or immune serum. Only the immune serum was able to reverse the antidiuretic and urine-concentrating effects of AVP, suggesting that the antibody antagonized the effects of AVP on the kidney. Taken together with the observation that this antibody did not bind to vasopressin, these data strongly indicate that an antibody to the vasopressin receptor binding site has been made and add further support to the molecular recognition theory.

Amino Acid Sequence↗
PubMed1989

Baroreflex function in lifetime-captopril-treated spontaneously hypertensive rats.

The effects of lifetime oral captopril treatment on baroreflex control of heart rate and lumbar sympathetic nerve activity were measured in 19-21-week-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). The sensitivity of baroreflex control of heart rate and lumbar sympathetic nerve activity were determined by the slopes of the relation between the change in mean arterial pressure (MAP) (mm Hg) versus the change in pulse interval (msec/beat) and the change in MAP versus the percent change in nerve activity, respectively. Untreated SHR had significantly higher MAP than WKY (157 +/- 3 vs. 115 +/- 3 mm Hg, p less than 0.001) and exhibited a decreased baroreflex control of heart rate. Lifetime treatment with captopril prevented the development of hypertension in SHR (MAP = 110 +/- 5 mm Hg) and increased the sensitivity of baroreflex function. The gains of the baroreflex control of heart rate for captopril-treated SHR and control SHR when MAP was raised or lowered by phenylephrine or nitroprusside were 2.38 +/- 0.49 vs. 1.10 +/- 0.33 msec/mm Hg (p less than 0.05) and 0.74 +/- 0.20 vs. 0.54 +/- 0.09 (NS) msec/mm Hg, respectively. The sensitivity of the baroreflex control of lumbar sympathetic nerve activity was greater in captopril-treated SHR than in control SHR when MAP was increased or decreased (-1.03 +/- 0.26 vs. -0.38 +/- 0.11, p less than 0.05; -0.84 +/- 0.2 vs. -0.04 +/- 0.58 (NS) mm Hg-1, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗