Release of the National Scheme's Aboriginal and Torres Strait Islander Health and Cultural Safety Strategy 2020-2025; the impacts for podiatry in Australia: a commentary.

BACKGROUND: Developing since colonisation, Australia's healthcare system has dismissed an ongoing and successful First Nations health paradigm in place for 60,000 years. From Captain James Cook documenting 'very old' First Nations Peoples being 'far more happier than we Europeans' and Governor Arthur Phillip naming Manly in admiration of the physical health of Gadigal men of the Eora Nation, to anthropologist Daisy Bates' observation of First Nations Peoples living 'into their eighties' and having a higher life expectancy than Europeans; our healthcare system's shameful cultural safety deficit has allowed for an Aboriginal and Torres Strait Islander child born in Australia today to expect to live 9 years less than a non-Indigenous child. Disproportionately negative healthcare outcomes including early onset diabetes-related foot disease and high rates of lower limb amputation in Aboriginal and Torres Strait Islander Peoples contribute to this gross inequity. MAIN BODY: In 2020, the Australian Health Practitioner Regulation Authority released the National Scheme's Aboriginal and Torres Strait Islander Health and Cultural Safety Strategy 2020-2025 - empowering all registered health practitioners within Australia to provide health care to Aboriginal and Torres Strait Islander Peoples that is inclusive, respectful and safe, as judged by the recipient of care. This recently released strategy is critically important to the podiatry profession in Australia. As clinicians, researchers and educators we have a collective responsibility to engage with this strategy of cultural safety. This commentary defines cultural safety for podiatry and outlines the components of the strategy in the context of our profession. Discussion considers the impact of the strategy on podiatry. It identifies mechanisms for podiatrists in all settings to facilitate safer practice, thereby advancing healthcare to produce more equitable outcomes. CONCLUSION: Aboriginal and Torres Strait Islander Peoples access health services more frequently and have better health outcomes where provision of care is culturally safe. By engaging with the National Scheme's Aboriginal and Torres Strait Islander Health and Cultural Safety Strategy, all registered podiatrists in Australia can contribute to achieving equity in health outcomes for Aboriginal and Torres Strait Islander Peoples.

Importance of imidazoline-preferring receptors in the cardiovascular actions of chronically administered moxonidine, rilmenidine and clonidine in conscious rabbits.

OBJECTIVE: To determine the involvement of central imidazoline receptors in the cardiovascular actions of the chronically administered antihypertensive agents moxonidine, rilmenidine and clonidine. DESIGN AND METHODS: In 21 rabbits with implanted fourth-ventricular catheters, we investigated the central effects of three cumulative doses of an I(1)-imidazoline/alpha(2)-adrenoceptor antagonist, efaroxan, and of an alpha(2)-adrenoceptor antagonist, 2-methoxyidazoxan (2-MI), on the changes in blood pressure and heart rate (HR) elicited by chronic subcutaneous administration of moxonidine, rilmenidine and clonidine, after 1 and 3 weeks of treatment. A low, medium and high dose of 2-MI was matched to three doses of efaroxan, such that each produced equal reversal of the hypotension induced by fourth-ventricular alpha-methyldopa and hence produced a similar degree of alpha(2)-adrenoceptor blockade. RESULTS: Clonidine and moxonidine, at doses of 1 mg/kg per day, and rilmenidine at 5 mg/kg per day, produced sustained reductions in mean arterial pressure of 13 +/- 3, 15 +/- 2 and 13 +/- 2 mmHg, respectively over the 3-week treatment period, but did not alter HR. Central administration of efaroxan on day 9 and day 23 of treatment produced a greater increase in blood pressure than did 2-MI with all three antihypertensive agents. Blood pressure reached levels that were significantly above the original control values. By contrast, the alpha(2)-adrenoceptor antagonist 2-MI only induced a rebound blood pressure effect in clonidine- and to a lesser extent in rilmenidine-treated rabbits. Both efaroxan and 2-MI produced a similar degree of tachycardia in moxonidine-, rilmenidine- and clonidine-treated animals.(2) CONCLUSIONS: The greater effect of efaroxan compared to the alpha(2)-adrenoceptor antagonist 2-MI suggests that the hypotension induced by chronic subcutaneous administration of moxonidine, rilmenidine and clonidine is mediated predominantly via an action on central imidazoline receptors. Furthermore, all agents showed a propensity to produce rebound hypertension with imidazoline receptor blockade. However, only clonidine showed a rebound phenomenon when challenged by acute central alpha(2)-adrenoceptor blockade

The rostral ventrolateral medulla mediates sympathetic baroreflex responses to intraventricular angiotensin II in rabbits.

The present study examined the role of the rostral ventrolateral medulla (RVLM) in mediating the pressor and renal sympathetic baroreflex effects of intraventricularly administered angiotensin II (Ang II) in urethane anaesthetised rabbits. Microinjection of Ang II over a wide range of medullary sites showed that pressor responses were observed only in the RVLM. Ang II was particularly potent in producing a transient pressor response at this site with a half maximal dose of 9 fmol. The administration of the Ang II antagonist Sar(1)-Ile(8)-Ang II (10 pmol) bilaterally into the RVLM inhibited the pressor response to local and fourth ventricular Ang II, but not the pressor response to RVLM applied glutamate. To determine the contribution of the RVLM to the renal sympathetic baroreflex effects of Ang II, blood pressure-renal sympathetic nerve activity (RSNA) curves were constructed with intravenous infusion of phenylephrine or nitroprusside before and after Ang II, vehicle or glutamate infusions into the RVLM. Ang II infusion of 4 pmol/min into the RVLM increased blood pressure by 8+/-3 mm Hg and shifted the renal sympathetic baroreflex curve to the right. The maximum RSNA evoked by lowering blood pressure increased by 36+/-6%, similar to the effect seen with fourth ventricular Ang II and RVLM glutamate. These studies suggest that the major medullary pressor site of action of Ang II when injected into the hindbrain cerebro-spinal fluid of anaesthetized rabbits is the RVLM where it facilitates baroreflex control of RSNA.