Rapid Hypertensinogenic Effect of Lead: Studies in the Spontaneously Hypertensive Rat
Chronic lead exposure may cause hypertension in normotensive rats. This hypertensinogenic effect has been attributed to perturbations in the renin-angiotensin axis, the contractile resporase of the vascular smooth muscle, or the intracellular Ca2+ homeostasis as a consequence of the inhibition of Na...
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| Veröffentlicht in: | Toxicology and industrial health 1992-01, Vol.8 (1-2), p.89-102 |
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| creator | Nakhoul, Farid Kayne, Laurie H. Brautbar, Nachman Hu, Ming-Shu Mcdonough, Alicia Eggena, Peter Golub, Michael S. Berger, Morris Chang, Chwen-Tzuei Jamgotchian, Nora Lee, David B.N. |
| description | Chronic lead exposure may cause hypertension in normotensive rats. This hypertensinogenic effect has been attributed to perturbations in the renin-angiotensin axis, the contractile resporase of the vascular smooth muscle, or the intracellular Ca2+ homeostasis as a consequence of the inhibition of Na+-K+-ATPase activity. In this study we examined the short-term effect of lead exposure on blood pressure, plasma renin activity, vascular contractility, and renal Na+-K+-ATPase activity and abundance in the spontaneously hypertensive rat. Our data indicate that modest lead exposure caused blood pressure elevation within two weeks in this rat strain that is genetically susceptible to the development of hypertension. This rapid blood pressure-elevating effect did not appear to depend on the mechanisms described in hypertension associated with more chronic lead exposure listed above. This acute model provides an additional approach to the study of lead-induced hypertension. |
| doi_str_mv | 10.1177/074823379200800108 |
| format | Article |
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This hypertensinogenic effect has been attributed to perturbations in the renin-angiotensin axis, the contractile resporase of the vascular smooth muscle, or the intracellular Ca2+ homeostasis as a consequence of the inhibition of Na+-K+-ATPase activity. In this study we examined the short-term effect of lead exposure on blood pressure, plasma renin activity, vascular contractility, and renal Na+-K+-ATPase activity and abundance in the spontaneously hypertensive rat. Our data indicate that modest lead exposure caused blood pressure elevation within two weeks in this rat strain that is genetically susceptible to the development of hypertension. This rapid blood pressure-elevating effect did not appear to depend on the mechanisms described in hypertension associated with more chronic lead exposure listed above. 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This hypertensinogenic effect has been attributed to perturbations in the renin-angiotensin axis, the contractile resporase of the vascular smooth muscle, or the intracellular Ca2+ homeostasis as a consequence of the inhibition of Na+-K+-ATPase activity. In this study we examined the short-term effect of lead exposure on blood pressure, plasma renin activity, vascular contractility, and renal Na+-K+-ATPase activity and abundance in the spontaneously hypertensive rat. Our data indicate that modest lead exposure caused blood pressure elevation within two weeks in this rat strain that is genetically susceptible to the development of hypertension. This rapid blood pressure-elevating effect did not appear to depend on the mechanisms described in hypertension associated with more chronic lead exposure listed above. This acute model provides an additional approach to the study of lead-induced hypertension.</description><subject>560300 - Chemicals Metabolism & Toxicology</subject><subject>ACID ANHYDRASES</subject><subject>ANIMALS</subject><subject>ATP-ASE</subject><subject>BLOOD PRESSURE</subject><subject>Body Weight</subject><subject>CARDIOVASCULAR DISEASES</subject><subject>CHRONIC EXPOSURE</subject><subject>DISEASES</subject><subject>ELEMENTS</subject><subject>ENVIRONMENTAL EXPOSURE</subject><subject>ENZYMES</subject><subject>Femoral Artery - physiology</subject><subject>HYDROLASES</subject><subject>HYPERTENSION</subject><subject>Hypertension - chemically induced</subject><subject>LEAD</subject><subject>Lead - blood</subject><subject>Lead - toxicity</subject><subject>Lead - urine</subject><subject>Male</subject><subject>MAMMALS</subject><subject>METALS</subject><subject>NONSPECIFIC PEPTIDASES</subject><subject>ORGANIC COMPOUNDS</subject><subject>PATHOGENESIS</subject><subject>PEPTIDE HYDROLASES</subject><subject>PHOSPHOHYDROLASES</subject><subject>PROTEINS</subject><subject>RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT</subject><subject>RATS</subject><subject>Rats, Inbred SHR</subject><subject>RENIN</subject><subject>Renin - metabolism</subject><subject>RODENTS</subject><subject>SYMPTOMS</subject><subject>TOXICITY</subject><subject>VASCULAR DISEASES</subject><subject>VERTEBRATES</subject><issn>0748-2337</issn><issn>1477-0393</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1992</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE9LJDEUxIMo7qz6BYSF4MVT60vSnXTvbRFdFwYE_5xDJnnRyEzSdtIL8-23hxZcEDwVvPeroihCThlcMKbUJai65UKojgO0AAzaPbJgtVIViE7sk8UOqHbEN_I951cAkLLhh-SQNTVv23ZBnu5NHxy93fY4FIw5xPSMMVh67T3aQpOnSzTuJ30oowuYaYi0vCB96FMsJmIa83r7n_0v0ntTjsmBN-uMJ-96RJ5urh-vbqvl3e8_V7-WlRWdKlUDnRMNBxQSjLPGO-a8b0AoLltp6hW3te2kU0ahqFcKvRGTWiW76bSS4oiczbkpl6CzDQXti00xTtV10zAuBUzQ-Qz1Q3obMRe9Cdniej3X10oCZ43i7UTymbRDynlAr_shbMyw1Qz0bnH9efHJ9OM9flxt0H1Y5omn_-X8z-YZ9WsahzhN8lXiP-G5iGA</recordid><startdate>199201</startdate><enddate>199201</enddate><creator>Nakhoul, Farid</creator><creator>Kayne, Laurie H.</creator><creator>Brautbar, Nachman</creator><creator>Hu, Ming-Shu</creator><creator>Mcdonough, Alicia</creator><creator>Eggena, Peter</creator><creator>Golub, Michael S.</creator><creator>Berger, Morris</creator><creator>Chang, Chwen-Tzuei</creator><creator>Jamgotchian, Nora</creator><creator>Lee, David B.N.</creator><general>SAGE Publications</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7U7</scope><scope>C1K</scope><scope>OTOTI</scope></search><sort><creationdate>199201</creationdate><title>Rapid Hypertensinogenic Effect of Lead: Studies in the Spontaneously Hypertensive Rat</title><author>Nakhoul, Farid ; Kayne, Laurie H. ; Brautbar, Nachman ; Hu, Ming-Shu ; Mcdonough, Alicia ; Eggena, Peter ; Golub, Michael S. ; Berger, Morris ; Chang, Chwen-Tzuei ; Jamgotchian, Nora ; Lee, David B.N.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c397t-509d3520e360adcafd1dff50372686a4b2c4c96d7a7e34b7efa334bc7697a7b63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1992</creationdate><topic>560300 - Chemicals Metabolism & Toxicology</topic><topic>ACID ANHYDRASES</topic><topic>ANIMALS</topic><topic>ATP-ASE</topic><topic>BLOOD PRESSURE</topic><topic>Body Weight</topic><topic>CARDIOVASCULAR DISEASES</topic><topic>CHRONIC EXPOSURE</topic><topic>DISEASES</topic><topic>ELEMENTS</topic><topic>ENVIRONMENTAL EXPOSURE</topic><topic>ENZYMES</topic><topic>Femoral Artery - physiology</topic><topic>HYDROLASES</topic><topic>HYPERTENSION</topic><topic>Hypertension - chemically induced</topic><topic>LEAD</topic><topic>Lead - blood</topic><topic>Lead - toxicity</topic><topic>Lead - urine</topic><topic>Male</topic><topic>MAMMALS</topic><topic>METALS</topic><topic>NONSPECIFIC PEPTIDASES</topic><topic>ORGANIC COMPOUNDS</topic><topic>PATHOGENESIS</topic><topic>PEPTIDE HYDROLASES</topic><topic>PHOSPHOHYDROLASES</topic><topic>PROTEINS</topic><topic>RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. 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This hypertensinogenic effect has been attributed to perturbations in the renin-angiotensin axis, the contractile resporase of the vascular smooth muscle, or the intracellular Ca2+ homeostasis as a consequence of the inhibition of Na+-K+-ATPase activity. In this study we examined the short-term effect of lead exposure on blood pressure, plasma renin activity, vascular contractility, and renal Na+-K+-ATPase activity and abundance in the spontaneously hypertensive rat. Our data indicate that modest lead exposure caused blood pressure elevation within two weeks in this rat strain that is genetically susceptible to the development of hypertension. This rapid blood pressure-elevating effect did not appear to depend on the mechanisms described in hypertension associated with more chronic lead exposure listed above. This acute model provides an additional approach to the study of lead-induced hypertension.</abstract><cop>Thousand Oaks, CA</cop><pub>SAGE Publications</pub><pmid>1542888</pmid><doi>10.1177/074823379200800108</doi><tpages>14</tpages></addata></record> |
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| ispartof | Toxicology and industrial health, 1992-01, Vol.8 (1-2), p.89-102 |
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| subjects | 560300 - Chemicals Metabolism & Toxicology ACID ANHYDRASES ANIMALS ATP-ASE BLOOD PRESSURE Body Weight CARDIOVASCULAR DISEASES CHRONIC EXPOSURE DISEASES ELEMENTS ENVIRONMENTAL EXPOSURE ENZYMES Femoral Artery - physiology HYDROLASES HYPERTENSION Hypertension - chemically induced LEAD Lead - blood Lead - toxicity Lead - urine Male MAMMALS METALS NONSPECIFIC PEPTIDASES ORGANIC COMPOUNDS PATHOGENESIS PEPTIDE HYDROLASES PHOSPHOHYDROLASES PROTEINS RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT RATS Rats, Inbred SHR RENIN Renin - metabolism RODENTS SYMPTOMS TOXICITY VASCULAR DISEASES VERTEBRATES |
| title | Rapid Hypertensinogenic Effect of Lead: Studies in the Spontaneously Hypertensive Rat |
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