Tags

Type your tag names separated by a space and hit enter

Transient induction of ANG II-dependent malignant hypertension causes sustained elevation of blood pressure and augmentation of the pressor response to ANG II in CYP1A1-REN2 transgenic rats.
Am J Med Sci. 2010 Jun; 339(6):543-8.AJ

Abstract

INTRODUCTION

Transgenic rats with inducible expression of the mouse Ren2 renin gene [strain name: TGR(Cyp1a1Ren2)] allow induction of various degrees of ANG II-dependent hypertension. Dietary administration of the aryl hydrocarbon indole-3-carbinol (I3C) at a dose of 0.15% induces a slowly developing form of ANG II-dependent hypertension, whereas dietary administration of a higher dose (0.3%) of I3C results in the development of ANG II-dependent malignant hypertension. Cessation of administration of 0.15% I3C results in the normalization of blood pressure, indicating the reversibility of hypertension induced by this dose of I3C. The present study was performed to determine if ANG II-dependent malignant hypertension is similarly reversible following cessation of dietary administration of 0.3% I3C.

METHODS

Cyp1a1-Ren2 rats (n = 6) were fed a normal diet containing 0.3% I3C for 11 days to induce malignant hypertension.

RESULTS

Cyp1a1-Ren2 rats induced with I3C exhibited pronounced increases in systolic blood pressure (SBP) (132 +/- 3-229 +/- 11 mm Hg, P < 0.001) and marked decreases in body weight (303 +/- 4-222 +/- 2 g, P < 0.001). When I3C administration was terminated, SBP decreased to 167 +/- 4 mm Hg (P < 0.01) and body weight increased to normal levels (309 +/- 2 g, P < 0.01) within 12 days. However, SBP remained significantly elevated (172 +/- 1 mm Hg, P < 0.01) for up to 3 weeks after termination of dietary administration of 0.3% I3C. In addition, the magnitude of the blood pressure response to intravenous bolus administration of 50 ng of ANG II (50 microL in volume) 3 weeks after cessation of dietary I3C administration was substantially higher than that observed in normotensive control rats (134 +/- 1 mm Hg, n = 6) not previously induced with 0.3% I3C (53 +/- 2 versus 38 +/- 3 mm Hg, P < 0.05).

CONCLUSIONS

The present findings demonstrate that transient induction of ANG II-dependent malignant hypertension results in prolonged elevations of arterial blood pressure and marked augmentation of the magnitude of the pressor response to ANG II in Cyp1a1-Ren2 transgenic rats.

Authors+Show Affiliations

Department of Physiology, Tulane University Health Sciences Center, New Orleans, Louisiana, USA.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

20375689

Citation

Howard, Catherine G., et al. "Transient Induction of ANG II-dependent Malignant Hypertension Causes Sustained Elevation of Blood Pressure and Augmentation of the Pressor Response to ANG II in CYP1A1-REN2 Transgenic Rats." The American Journal of the Medical Sciences, vol. 339, no. 6, 2010, pp. 543-8.
Howard CG, Mullins JJ, Mitchell KD. Transient induction of ANG II-dependent malignant hypertension causes sustained elevation of blood pressure and augmentation of the pressor response to ANG II in CYP1A1-REN2 transgenic rats. Am J Med Sci. 2010;339(6):543-8.
Howard, C. G., Mullins, J. J., & Mitchell, K. D. (2010). Transient induction of ANG II-dependent malignant hypertension causes sustained elevation of blood pressure and augmentation of the pressor response to ANG II in CYP1A1-REN2 transgenic rats. The American Journal of the Medical Sciences, 339(6), 543-8. https://doi.org/10.1097/MAJ.0b013e3181d82a62
Howard CG, Mullins JJ, Mitchell KD. Transient Induction of ANG II-dependent Malignant Hypertension Causes Sustained Elevation of Blood Pressure and Augmentation of the Pressor Response to ANG II in CYP1A1-REN2 Transgenic Rats. Am J Med Sci. 2010;339(6):543-8. PubMed PMID: 20375689.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Transient induction of ANG II-dependent malignant hypertension causes sustained elevation of blood pressure and augmentation of the pressor response to ANG II in CYP1A1-REN2 transgenic rats. AU - Howard,Catherine G, AU - Mullins,John J, AU - Mitchell,Kenneth D, PY - 2010/4/9/entrez PY - 2010/4/9/pubmed PY - 2010/6/19/medline SP - 543 EP - 8 JF - The American journal of the medical sciences JO - Am. J. Med. Sci. VL - 339 IS - 6 N2 - INTRODUCTION: Transgenic rats with inducible expression of the mouse Ren2 renin gene [strain name: TGR(Cyp1a1Ren2)] allow induction of various degrees of ANG II-dependent hypertension. Dietary administration of the aryl hydrocarbon indole-3-carbinol (I3C) at a dose of 0.15% induces a slowly developing form of ANG II-dependent hypertension, whereas dietary administration of a higher dose (0.3%) of I3C results in the development of ANG II-dependent malignant hypertension. Cessation of administration of 0.15% I3C results in the normalization of blood pressure, indicating the reversibility of hypertension induced by this dose of I3C. The present study was performed to determine if ANG II-dependent malignant hypertension is similarly reversible following cessation of dietary administration of 0.3% I3C. METHODS: Cyp1a1-Ren2 rats (n = 6) were fed a normal diet containing 0.3% I3C for 11 days to induce malignant hypertension. RESULTS: Cyp1a1-Ren2 rats induced with I3C exhibited pronounced increases in systolic blood pressure (SBP) (132 +/- 3-229 +/- 11 mm Hg, P < 0.001) and marked decreases in body weight (303 +/- 4-222 +/- 2 g, P < 0.001). When I3C administration was terminated, SBP decreased to 167 +/- 4 mm Hg (P < 0.01) and body weight increased to normal levels (309 +/- 2 g, P < 0.01) within 12 days. However, SBP remained significantly elevated (172 +/- 1 mm Hg, P < 0.01) for up to 3 weeks after termination of dietary administration of 0.3% I3C. In addition, the magnitude of the blood pressure response to intravenous bolus administration of 50 ng of ANG II (50 microL in volume) 3 weeks after cessation of dietary I3C administration was substantially higher than that observed in normotensive control rats (134 +/- 1 mm Hg, n = 6) not previously induced with 0.3% I3C (53 +/- 2 versus 38 +/- 3 mm Hg, P < 0.05). CONCLUSIONS: The present findings demonstrate that transient induction of ANG II-dependent malignant hypertension results in prolonged elevations of arterial blood pressure and marked augmentation of the magnitude of the pressor response to ANG II in Cyp1a1-Ren2 transgenic rats. SN - 1538-2990 UR - https://www.unboundmedicine.com/medline/citation/20375689/Transient_induction_of_ANG_II_dependent_malignant_hypertension_causes_sustained_elevation_of_blood_pressure_and_augmentation_of_the_pressor_response_to_ANG_II_in_CYP1A1_REN2_transgenic_rats_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0002-9629(15)31578-0 DB - PRIME DP - Unbound Medicine ER -