LAGREW, J. P.; KRETZER, J.; LAWRENCE, C.; MALIK, D.; MATER, M.; BRUECKNER, J. K. Unilateral double plantaris muscle: a rare anatomical variation. Int. J. Morphol., 28(4):1097-1099, 2010. SUMMARY:The occurrence of a unilateral second plantaris muscle was discovered during the anatomical dissection of a 47 year old female with Huntington Chorea Disease. The cadaver was found to possess bilateral plantaris muscles and a distinct anomalous muscle morphologically resembling a second plantaris on the medial right leg. The inner and outer bellies of the anomalous plantaris arose proximally from the medial condyle of the femur and formed a short tendon that fused distally with the tendon of the lateral plantaris muscle.
Angiotensin II (AII) has been linked as a causal factor in several experimental models of hypertension (HT) including Okamoto spontaneously hypertensive rats (SHR). The transmission and expression of AII type 1 receptors (AT1r) in SHR and the development of genetic HT remain unknown. It is hypothesized that tissue-specific expression of renin–angiotensin system (RAS) genes derived from SHR are linked to HT in offspring of SHR crossed with Brown Norway (BN) rats. Hypertensive female progeny of BN/SHR matings was backcrossed with founder BN males to generate the F1 and five backcross generations (BN/SHR-mtSHR). Progeny were phenotyped according to normotension (NT: systolic arterial pressure [SAP] ≤ 124 mmHg), borderline hypertension (BHT: 124 ≤ SAP < 145 mmHg), and HT (SAP ≥ 145 mmHg). Six generations produced more HT (n = 88; 46%) than NT (n = 21; 11%) offspring. The mRNA expression of the RAS was evaluated in NT (n = 20) and HT (n = 20) BN/SHR-mtSHR across several generations. Quantitative real-time polymerase chain reaction analysis of kidney tissue showed increased expression of AII, type 1 receptors (Agtr1a) (∼2.5-fold) in HT versus NT rats, while other members of both the renal and systemic RAS pathway were not different. Western blot analysis from kidney homogenates showed that AT1r protein levels were higher (P < 0.05) in backcross generation 3 (BC3) HT versus NT rats. Evaluation of SAP as a function of AT1r expression by linear regression indicated positive correlation (P < 0.05) in kidney of BC3 BN/SHR-mtSHR rats. Thus, elevated kidney AT1r expression may be involved in the development of HT in BN/SHR-mtSHR rats.
Low frequency renal nerve stimulation (LFRNS) decreases medullary (MBF) and cortical (CBF) blood flows. The impact of endogenous nitric oxide (NO) on LFRNS mediated changes in MBF and CBF was determined in anesthetized Sprague Dawley (SD) rats. Animals (n=13) were anesthetized and Laser Doppler flow probes were positioned on or below the kidney surface to measure CBF and MBF. After control, LFRNS was conducted at 0.5 and 1.5 Hz for 15 minutes each. LFRNS (0.5 Hz) decreased MBF by ‐1.89 ± 0.39% and CBF by ‐2.12 ± 0.77% of control. At 1.5 Hz, LFRNS decreased MBF and CBF by ‐8.70+2.31% and ‐10.84 ± 3.7% of control, respectively. Following a 30 minute recovery period from LFRNS, L‐arginine (L‐ARG; 300 ug/kg/hr, i.v.) was infused for 30 minutes and LFRNS was repeated. L‐ARG infusion did not change control MBF or CBF but abolished renal vasoconstriction elicited by 0.5 Hz LFRNS. Furthermore, 1.5 Hz LFRNS mediated vasoconstriction was attenuated in both medullary and cortical regions (‐3.75 ± 1.78% and ‐6.87 ± 2.67%, respectively; p<0.05 vs. control constrictor responses). Thus, endogenous NO significantly decreases renal vascular constriction during LFRNS in renal medullary and cortical vessels. NO may provide protection against both cortical and medullary vasoconstriction during small and subtle changes in renal sympathetic outflow. (Supported by an APS Predoctoral Fellowship to J. Kretzer and UK Biology Ribble Foundation).
Angiotensin II type 1 receptor (AT1r) expression is increased in genetic models of hypertension including the Okamoto Spontaneously Hypertensive Rat (SHR). This study evaluated tissue AT1r expression compared to arterial blood pressure of F1 generation offspring of SHR female crossed with Brown Norway (BN) male rats. Systolic and diastolic arterial pressures were measured by tail cuff plethysmography and mean arterial pressure (MAP) was calculated. Offspring were sacrificed at 15‐20 weeks of age and tissues were rapidly frozen for analysis of AT1r. MAP of parent, female SHR was 151 mmHg and parent male BN was 94 mmHg. F1 generation offspring were produced from 6 separate matings of SHR and BN parents. Blood pressures of F1 offspring were measured at 14‐17 weeks of age. F1 progeny were grouped according to borderline hypertension (BHT; MAP < 122 mmHg; n=18) and hypertension (HT; MAP > 122 mmHg; n=15). All progeny exhibited MAPs greater than 107 mmHg. Total tissue protein was extracted from forebrain, hypothalamus and kidney tissues and separated by gel electrophoresis. Western blot analysis was conducted for AT1r. In F1 SHR/BN, there were no detectable differences in AT1r between BHT and HT animals. Hypertension in SHR is dominantly expressed when crossed with NT‐BN. The data suggest that differences in MAP of F1 BHT and HT SHR/BN are not mediated by altered AT1r expression. (Supported by UK Biology Ribble Foundation)
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.