Dr David H. Robertson, the Elton Yates Professor of Autonomic Disorders and founder of the Vanderbilt Autonomic Dysfunction Center and the American Autonomic Society, peacefully passed away on January 12, 2024, in Nashville, TN surrounded by his family (Figure).

Figure. Dr David H. Robertson, Elton Yates Professor of Autonomic Disorders, Vanderbilt University Medical Center, 1947 to 2024.

David graduated from Vanderbilt University in 1969 in Germanic and Slavic Languages and became interested in medicine during his undergraduate years. After graduating from Vanderbilt, he attended the Arnamagnane Institute in Copenhagen, Denmark, pursuing his interest in the Icelandic language. Then, he returned to Nashville to attend the Vanderbilt School of Medicine and received his medical degree in 1973. David completed his internship and residency at Johns Hopkins Hospital and was a postdoctoral fellow in the Division of Clinical Pharmacology at Vanderbilt before accepting his position as assistant chief of service in medicine and instructor in medicine at John Hopkins in 1977. Then, he returned to Vanderbilt to pursue his academic career.

David was a caring physician, a brilliant patient-oriented investigator, and an outstanding mentor. Early in his career, David developed an interest in autonomic control of the circulation. He established unique and highly innovative clinical and translational strategies to study autonomic function, ultimately making seminal contributions to understanding the role of the sympathetic nervous system in hypertension and to the treatment of autonomic disorders.

David established the Vanderbilt Autonomic Dysfunction Center, which continues today as a leading center for the treatment of autonomic disorders. He assembled a team of outstanding physicians, scientists, and staff and developed a highly sophisticated infrastructure that allowed multiple measures of autonomic function in humans and experimental animals. An example of his scholarship and accomplishment was his discovery of dopamine-β-hydroxylase deficiency. Patients with this condition present with orthostatic hypotension and orthostatic tachycardia due to isolated sympathetic failure, with intact parasympathetic function. David deduced that they suffered from dopamine-β-hydroxylase deficiency,¹ after confirming that sympathetic nerves and autonomic reflexes were preserved by measuring muscle sympathetic nerve activity,² and that dopamine, instead of norepinephrine, acted as the neurotransmitter from sympathetic nerves. He showed that both the excess dopamine and loss of norepinephrine contributed to orthostatic hypotension.³ In addition, he discovered that droxidopa could detour the enzymatic defect and restore endogenous levels of norepinephrine,⁴ becoming the first cure for an autonomic disorder with complete resolution of the illness.⁵ This work led to droxidopa being the second drug approved by the US Food and Drug Administration for the treatment of orthostatic hypotension.^6–8 Droxidopa is now commonly used for other causes of orthostatic hypotension, and has improved the quality of life for humans with these disorders.

David was an excellent clinician, observant, and listener of the patient’s symptoms. During his lectures to medical students and fellows, he often taught, “Patient-oriented research occurs when the patient and the scientist are both in the room at the same time, and both are alive.” He described the hypotensive effect of meals (postprandial hypotension) after his patients complained of worsening of symptoms after eating,⁹ and developed novel treatment with either caffeine or acarbose.^10,11 David also discovered the pressor effect of water after an anecdotal encounter with a patient, who reported feeling better after drinking a bolus of water¹²; this novel autonomic reflex had not previously been recognized by autonomic neuroscientists.¹³ He found a clinical use for this reflex as a rescue measure in patients with orthostatic hypotension because of its potency and fast onset.¹⁴ These clinical observations were further studied in the laboratory using elegant mouse models to characterize hypoosmolality and Trpv4 receptors in the portal circulation as the trigger for this pressor effect.¹⁵

David and his team also discovered the clinical phenotype of afferent baroreflex failure. This condition is characterized by extreme labile hypertension caused by excessive, unrestrained sympathetic activity in patients with baroreceptor damage caused by surgery or radiation.¹⁶ Using elegant biochemical and pharmacological testing he described a subset of patients with orthostatic hypotension and malignant vagotonia, who had preserved cardiac vagal efferent activity.¹⁷

David was also responsible for discovering one of the first congenital conditions associated with Postural Tachycardia Syndrome. By studying 2 sisters with postural tachycardia, he recognized a distinct biochemical pattern of elevated plasma norepinephrine levels and decreased plasma dihydroxyphenylglycine levels. David recognized that this was consistent with impaired norepinephrine reuptake, and discovered this was due to a variant of the norepinephrine transporter gene (SLC6A2).^18,19 Knowledge of the importance of the norepinephrine transporter led to the discovery of norepinephrine transporter inhibitors for treating orthostatic hypotension.^20–23

These discoveries are just a glimpse of his many contributions to science and patient care.

David shaped the future of modern clinical autonomic medicine by defining these autonomic syndromes, their clinical evaluation, and treatment. His book “Primer on the Autonomic Nervous System” has been the premier text for autonomic disorders since 1996. David mentored >30 fellows, many of who now occupy academic leadership positions in the United States and abroad. He was also the Principal Investigator for the Autonomic Rare Diseases Clinical Research Consortium and the Editor for the Spotlight on Rare Diseases, which is the newsletter of the National Institutes of Health Rare Disease Clinical Research Consortia. David also served as Director of the Center for Space Physiology and Medicine at Vanderbilt.

Of the numerous awards David received during his career, he particularly cherished the Irvine Page and Alva Bradley Lifetime Achievement Award bestowed by the Council on Hypertension in 2016.

Foremost, David was loved by his patients, he recognized the importance of patient and caregiver engagement and fostered the Shy-Drager Support Group (now MSA Coalition) in 1989. David is survived by his wife Dr Rose Marie Robertson, Deputy Chief Science and Medical Officer of the American Heart Association, and their daughter Rose Marie Robertson Pink.

None.

Disclosures None.

For Sources of Funding and Disclosures, see page e45.

埃尔顿·耶茨 (Elton Yates) 自主神经疾病教授、范德比尔特自主神经功能障碍中心和美国自主学会创始人 David H. Robertson 博士于 2024 年 1 月 12 日在田纳西州纳什维尔在家人的陪伴下平静地去世（图）。

数字。 David H. Robertson 博士，范德比尔特大学医学中心埃尔顿·耶茨自主神经疾病教授，1947 年至 2024 年。

David 于 1969 年毕业于范德比尔特大学日耳曼和斯拉夫语言专业，并在本科期间对医学产生了兴趣。从范德比尔特大学毕业后，他进入丹麦哥本哈根的 Arnamagnane 学院，追求对冰岛语言的兴趣。然后，他返回纳什维尔进入范德比尔特医学院，并于 1973 年获得医学学位。大卫在约翰·霍普金斯医院完成了实习和住院医师实习，并在接受助理职位之前在范德比尔特临床药理学部担任博士后研究员1977 年，他成为约翰霍普金斯大学的医学服务主任和医学讲师。然后，他回到范德比尔特继续他的学术生涯。

大卫是一位充满爱心的医生，一位出色的以患者为中心的调查员，也是一位杰出的导师。在他职业生涯的早期，大卫对循环的自主控制产生了兴趣。他建立了独特且高度创新的临床和转化策略来研究自主神经功能，最终为理解交感神经系统在高血压中的作用和治疗自主神经紊乱做出了开创性贡献。

大卫建立了范德比尔特自主神经功能障碍中心，该中心至今仍是治疗自主神经疾病的领先中心。他组建了一支由杰出医生、科学家和工作人员组成的团队，并开发了高度复杂的基础设施，可以对人类和实验动物的自主功能进行多种测量。他的学术和成就的一个例子是他发现了多巴胺-β-羟化酶缺乏症。这种情况的患者由于孤立性交感神经衰竭而出现直立性低血压和直立性心动过速，但副交感神经功能完整。大卫通过测量肌肉交感神经活动确认交感神经和自主反射得以保留， ²并且多巴胺而不是去甲肾上腺素充当了交感神经的神经递质，因此推断他们患有多巴胺-β-羟化酶缺乏症， ¹ 。他表明，过多的多巴胺和去甲肾上腺素的减少都会导致体位性低血压。 ³此外，他还发现屈昔多巴可以绕过酶促缺陷并恢复去甲肾上腺素的内源水平， ⁴成为第一个完全治愈自主神经疾病的疗法。 ⁵这项工作使屈昔多巴成为美国食品和药物管理局批准的第二种用于治疗直立性低血压的药物。 ^6–8屈昔多巴现在常用于治疗其他原因引起的直立性低血压，并改善了患有这些疾病的人的生活质量。

大卫是一位出色的临床医生、患者症状的观察者和倾听者。在给医学生和研究员讲课时，他经常说：“当患者和科学家同时在房间里，并且都还活着时，就会发生以患者为导向的研究。”在他的患者抱怨进食后症状恶化后，他描述了进餐的降血压作用（餐后低血压） ⁹ ，并开发了咖啡因或阿卡波糖的新疗法。 ^10,11 David 在与一位患者的一次轶事接触后还发现了水的升压作用，该患者报告说喝了一大团水后感觉好多了¹² ；这种新颖的自主神经反射此前并未被自主神经科学家所认识。 ¹³他发现这种反射在临床上可作为直立性低血压患者的抢救措施，因为其效力强且起效快。 ¹⁴这些临床观察结果在实验室中使用优雅的小鼠模型进行了进一步研究，以表征门静脉循环中低渗性和 Trpv4 受体作为这种升压效应的触发因素。 ¹⁵

大卫和他的团队还发现了传入压力反射失败的临床表型。这种疾病的特点是因手术或放射造成压力感受器损伤的患者交感神经活动过度、不受限制而引起极度不稳定的高血压。 ¹⁶通过优雅的生化和药理学测试，他描述了一组患有直立性低血压和恶性迷走神经症的患者，这些患者保留了心脏迷走神经传出活动。 ^{17 号}

大卫还发现了与姿势性心动过速综合征相关的第一个先天性疾病之一。通过研究两名患有体位性心动过速的姐妹，他发现了血浆去甲肾上腺素水平升高和血浆二羟苯基甘氨酸水平降低的独特生化模式。 David 认识到这与去甲肾上腺素再摄取受损一致，并发现这是由于去甲肾上腺素转运蛋白基因 ( SLC6A2 ) 的变异所致。 ^18,19对去甲肾上腺素转运蛋白重要性的认识促使人们发现了用于治疗直立性低血压的去甲肾上腺素转运蛋白抑制剂。 ^20–23

这些发现只是他对科学和患者护理做出的众多贡献的冰山一角。

大卫通过定义这些自主神经综合征、其临床评估和治疗，塑造了现代临床自主医学的未来。自 1996 年以来，他的著作《自主神经系统入门》一直是有关自主神经疾病的首要著作。David 指导过超过 30 名研究员，其中许多人现在在美国和国外担任学术领导职务。他还是自主罕见疾病临床研究联盟的首席研究员，以及美国国立卫生研究院罕见疾病临床研究联盟的通讯《罕见疾病聚焦》的编辑。大卫还担任范德堡大学空间生理学和医学中心主任。

在 David 职业生涯中获得的众多奖项中，他特别珍惜 2016 年高血压委员会授予的欧文·佩吉 (Irvine Page) 和阿尔瓦·布拉德利 (Alva Bradley) 终身成就奖。

最重要的是，David 深受患者喜爱，他认识到患者和护理人员参与的重要性，并于 1989 年成立了 Shy-Drager 支持小组（现为 MSA 联盟）。David 身后留下了他的妻子 Rose Marie Robertson 博士，她是科学和医疗副主任美国心脏协会官员和他们的女儿罗斯·玛丽·罗伯逊·平克。

 没有任何。

披露无。

有关资金来源和披露信息，请参阅第 e45 页。